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This Is Washington State No. 11 - Port Townsend Light House by Paul W Sharpe Aka Wizard of Wonders - 8.000" x 4.375"
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Light House overlooks the small town of Port Townsend and inner passage of Puget Sound, Washington state, USA
"I like to think, I see the world, how most do not" If you would like to purchase one of my images for website or commercial use including Rights Managed images please visit my website www.wizardofwonders.com Any of my images are available in Color or Black and White please email me with your requests and i will wave my magic wand. Biography Paul W Sharpe aka Wizard of Wonders is a visual artist. His art is about deep thinking dimensions, which takes viewers in another spaces, another dimension of our brain, with employing chaotic geometrical elements. Esthetic and composition became a new definition in his artwork so a viewer will be challenged with the classical understanding of art. The...
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(written from a Production point of view)
Carla Lewis is a casting director who hired background performers for Star Trek. [1] [2] She is the co-founder of Hollywood Operating Systems (or Hollywood OS) and is currently the head of Headquarters Casting, "a full service principal and background talent casting agency." [3] In February 2012, Lewis and Headquarters Casting have open casting calls for background performers for the Star Trek Into Darkness. [4]
Lewis has also cast background performers for such films as Lords of Dogtown, Failure to Launch, The Fast and the Furious: Tokyo Drift, Knocked Up, and Georgia Rule. She recently wrapped up work on National Treasure: Book of Secrets. In addition to Star Trek, she is casting extras for Ben Stiller's Tropic Thunder and the upcoming ABC series Miss/Guided. She also continues to work as casting director on Jimmy Kimmel Live!
Webster (and Headquarters Casting) oversaw an open casting call for extras for Star Trek at the Hollywood OS office in Burbank, California on 10 November 2007. They were looking for people to play Vulcans and cadets. They are seeking "thin, athletic men and women, ages 18-90", particularly those with "interesting and unique facial features." [5] Hundreds of people – both fans and actors just looking for work – attended the casting call. [6]
External links Edit
- HeadquartersCasting.com – official site
- HollywoodOS.com – official site
- Carla Lewis at IMDb


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Sunday, April 25, 2010
Art of Living = Money, sex, scam, fraud, deceit
Is the Art of Living Foundation a scam? Is Sri Sri Ravi Shankar a fraud?
Maharishi Mahesh Yogi called Ravi Shankar "sugar coated poison". That kind of sums it.
The latest is that in his current US tour, RS (Ravi Shankar) is summoning his people to raise more money, get to the wealthy, for another project, Sri Sri University. Another scam! Raise money from others using volunteers (who do it for free and sacrifice their life, rather than earn it for themselves) and then invest it in property who's beneficiaries are his family members and use the front of Sri Sri University! Wow! that the best model in the world don't you think? Very similar to that of Maharishi his master. They say the devotee out does the master!
Before the Nithyananda scandal broke out, Rajshree Patel, the executive director of the Art of Living LA Center went and met Popat Savla, the head of the Nithyananda org. in LA. Mr Savla then mailed Rajshree a $50,000 check!
He gave $2.5mil to Nithyananda to buy and build the temple in LA. Even after the scandal broke out Sri Sri had the guts to visit them in LA. You all read the article in the Deccan Herald about Sri Sri going to visit the Nithyananda temple and Mr. Savla contacted the newspaper and told them if felt like a corporate takeover. Yes, he's a good candidate for take over since he gave millions in the past.
After going past the "sugar" it takes wisdom to recognize the "poison". I am eagerly waiting to read more articles from Whistleblower on the deep dark secrets of Sri Sri. I hope that all of you read Whistleblowers extremely intriguing comments under the post Comment on the "Teacher's pompous answer to a devotee's sincere question."
18 comments:
Sri Sri's take on IPL: Needs more cleaning than Yamuna
"Sports should simply bring lightness, laughter and entertainment. When business enters it, its very soul is destroyed," Sri Sri, as he is called fondly by his worldwide devotees, said in a statement here Sunday.
- April 26, 2010 at 2:01 AM
Some of the comments below that said article in Deccan Herald spew of vitriol:
"why shd sri sri even comment abt IPL ?? if he is a sashu / spiritual guru he shd not be getting involved in wordly matters .sure he art of living oo neds an audit . govt shd pass an act stating that all ashrams will be subject to audit ..sri sri was the one who was seen in a compromising pose on an aircraft some years ago ..."
These are people who probably haven't even taken AOL's courses..hmm maybe public perception is changing?? Klim, do you know anything about this so called compromising photo in an airplane?
- April 26, 2010 at 11:35 AM
I wonder if dictators like Hitler, Mao Zedong or Stalin, who caused so much sufferings to mankind, reincarnate into Sri Sris, Nithyas or characters of the kind? There is so much similarity. On the other hand, ideas of Hitler, Mao or Stalin manifested only because of the help of their followers.
No trial provides a better basis for understanding the nature and causes of Evil than do the Nuremberg trials from 1945 to 1949. Those who come to the trials expecting to find sadistic monsters are generally disappointed. What is shocking about Nuremberg is the ordinariness of the defendants: men who may be good fathers, kind to animals, even unassuming--yet who committed unspeakable crimes. In most cases, the defendants themselves took the stand, trying to put their actions in as positive of a light as possible. Many of the defendants claimed to know nothing of the existence of concentration camps or midnight killings. Other defendants used their testimony to emphasize that they were merely following orders.
Devotees, are you "merely follow orders of the Master"? No, YOU are responsible. It is with your help that money laundering, stealing, fraud and deceit take place.
- April 26, 2010 at 12:57 PM
NEed of the hour= Get the URL of this blog published in deccan herald. I mean it.
- April 26, 2010 at 1:29 PM
Gosh! The blog war has started! :)
Now Ravi Shankar has asked his followers to start a blog "Exposing the Guruholic" http://artoflivingfreefree.blogspot.com.
What a joke!
And the followers are none other than Harish Ramachandran, CEO of Sumeru Solutions, an Art of Living, or should I say Bhanu didi-Narshimhan Company and one of the biggest scams of Ravi Shankar. And the other follower is Harish's wife Bharathy! Wow! how stupid and childish can Art of Living folks get!
They have now posted this blog on the Deccan Herald article mentioned above...and when someone posts this blog (by KLIM) in the comments section for an article online, say Deccan Herald, Art of Living marketing machine Reports it as Abuse! They need a life!
- April 26, 2010 at 1:36 PM
Thanks Anon 1:36 pm for alerting us to SriSri's new blog.
What a joke! Right from its first post is deceitful, claiming:
"The Art of Living doesn't seem to be doing much about countering these allegations, in fact this is one of their policies i don't agree with, so I decided to do it."
These people are so pathetic! Not a truthful bone in their bodies!
KLIM congratualation. Obviously too much truth coming out in your blog, so Bhanu Didi & SriSri trembling already.
This is the biggest compliment they could have paid to you & greatest confirmation that you are on the right trail. No amount of such damage control is going to stop the torrent of evidence coming out & exposing AOL/SriSri & his lackeys for who they really are.
Congratulation KLIM & keep up the good work.
I, for one, am very happy for srisri/AOL creating that trash of a blog & hope all the lackeys now go & post their comments there & leave this blog alone.
And yes, they have every right to be scared, because once truth comes out srisri will join the ranks of Nithyananda & other such disgraced Gurus.
And KLIM look at their blog as free advertisement. I was thinking how we can alert all AOL centres & members & pass your blog url to them. Here it is SriSri & his lackeys doing the job for us, mentioning Guruhloic by name & even their blog's name is based on yours. Wow Sumeru solutions, never thought we would get any free help from you guys to promote our blog!Keep up the good work. We can do with all free promotion!
- April 26, 2010 at 4:47 PM
Rajshree Patel in US & her brother Kamlesh Patel in Europe are just more of SriSri's lackeys & in the same league as Bawa & Dinesh.
They also take huge sums of money from AOL. Just like SriSri, AOL is a very profitable business for them.
They deceive people & raise a lot of money from unsuspected business & organisations in the name of charity, they then take a sizeable portion for themselves & rest goes to RS coffers. They live off AOL! THEY ARE NOT VOLUNTEER UNPAID WORKERS. They just train unpaid volunteers workers for SriSri. Young men & women are persuaded to forgo their lives, education & career & instead do slave labour for SriSri & the money they raise goes to fund SriSri , his family & his lackeys lifestyle. Look where SriSri's nephews live & study & how many property they have bought from the money all innocent volunteers send to AOL for so called charitable projects!
Sri Sri looks after his lackeys & they promote him. Again they know each others dark secrets so they feel pretty safe with each other and as the saying goes have their hands in each other's pocket.
Kamlesh has been heard to tell attractive women to use their "feminity" to buy influence for SriSri. I once had to console a young woman who was deeply hurt & felt insulted from such comment. Obviously Kamlesh thought other women would like to operate same way as his sister. And have you seen Kamlesh when he gets angry? Not a pretty sight! Seems runs in the family! Knowledge points they only preach to others, no sign of them practicing it themselves.
The only times I have seen them using knowledge points were either to attack someone or justify themselves when they were caught with their pants down. As to practise Sadhna, again it is only when they teach it to innocent people, otherwise those who have lived with these guys know Sadhna is not part of their daily routine. Kamlesh even boasts about not needing Sadhna or adv courses! He even proudly talks how he even didn't finish basic course. All he cares about is $$$ & buying political influences for SriSri. He brags about how much he has fleeced Mittal family & other extra-rich Indian families in Europe. Then goes around & mucks them behind their back about what a show off they are re their wealth & how easily they part with $$$ to get SriSri's blessing!
Rajshree & Kamlesh have no integrity. They just have sold their soul to SriSri & getting paid hefty sums for their services.
All of us have responsibility to expose SriSri & his lackeys. Many innocent people are deceived & hurt by them. And see how the more corrupt & deceitful lackeys are the more they get promoted. That is why Rajshree became TTC teacher & blessing course teacher, not because she is spiritually advanced!!
- April 26, 2010 at 5:34 PM
What a fun? Artoflvingfreefree. so, like srisri, it is freefree. Come-on, AOL-Guys, Wake up. A true saint should be not be perturbed by any blemish to him. He should stand tall amidst all the critics. He should not explicitly justify and justification should be felt automatically. The new blog itself exposes that SRISRI is just a normal person who cannot stand critics. So the truth of klim's blog gets strengthened.
- April 27, 2010 at 12:12 AM
In case "J" is reading, here's something for you, as a comment on your blog, from me:
""True, sometimes some volunteers or teachers may be rude or sloppy in their behaviour" ????? Teachers? So these are the kind of teachers that are churned out? Those that "could be rude or sloppy"? Let them be called students then, not teachers.
Everyone knows that AoL is just watered down spirituality. Nothing is serious, there is no sense of spiritual purpose and there are always hormone propelled youngsters looking to get lucky at satsangs. It's so cheap.
FYI, artoflivingfree.blogspot.com is a very fair website and never used any degrading language. Obviously you guys are afraid, which is why this laughable blog started. If you truly claim to be as fair as you are, publish this post and let everyone find out for themselves what the truth is. TRUTH SHOULD PREVAIL. LIGHT WILL AUTOMATICALLY FOLLOW."
- April 27, 2010 at 2:07 AM
Comparing gurus like Ravi Ravi, Nithya and Sly Baba to Hitler, Stalin or Mao would be too much of a stretch. Autocrats and megalomaniacs abound everywhere. You can see such qualities in school teachers, CEOs, Managers, priests or anyone in positions of power. But by no stretch of imagination they are hitlers or maos who killed millions. We should bring a proper perspective to the Guru crimes of financial irregularities and abuse so that they can be investigated. Let's be realistic.
- April 27, 2010 at 2:14 AM
Regarding the new free free blog, they certainly have a right to defend AoL and to counter things written here. The purpose of this blog as I understand from reading is for healing, support and to give people a compassionate space to share their stories. Many sincere people on this blog have come forward and courageously shared their stories which have incidentally helped a lot of others including myself in various ways. The new blog is just a blip on the screen after what some people have been through with this cult.
I think you can tell a lot by a person from their blog. I also believe the truth will prevail. So, I say more power to that blogger--it's a free world! But, change the name please. It reminds me of Sri Sri which I always thought sounded just plain weird.
- April 27, 2010 at 10:02 AM
@ Upendra
Thank you for your comment. I agree that comparing SR and Nithya with Hitler and Stalin is too much. But in no way they are just like school teacher, CEOs, priests and other people, who abuse their position of power. All the above mentioned characters wanted and still want to impose their ideas to the world , and they make all effort to spread them, like cancer, to other countries by whatever means. All these people created a cult around their personalities (their pictures hanging in all places, songs are sung to honor them, slogans like "Heil Hitler" are supposed to be chanted by all the followers etc.). They all wanted and want ultimate obedience of the masses. Means to achieve this may be different: physical extermination, or just turning people into brainless obedient robots. These are just different flavors of EVIL, don't you think?
- April 27, 2010 at 12:59 PM
i so agree with chris william -
"hormone propelled youngsters looking to get lucky at satsangs. It's so cheap"
its not cheap its dirty filthy sick.
spirituality and sex - i shall soon post the details of one such guy who sings in satsangs gets a lot of attention and all this fame he uses to sleep around with girls under the innocent cover of guru grace.
i am gonna expose one such guy real soon..and i know the day i mention his name here...ssrs n the bhanu ma etc etc will make sure tat the young singer gets even more fame and publicity just to prove the so called guru grace on a satsang singer..
ssrs n whole of aol is fighting for bigger causes , call this aol as a family vasudeva kutumbh... while its a pity and shame that the family accepts and encourages and protects guys who rape and use aol platform for their personal benefits..even if they sing satsangs so what...rape is crime..using and abusing girls is a crime whether u have sex before or after satsang...
and to top it all ssrs makes strong comments on hussain's painting nude women..well well those r just paintings and here a real human a girl is raped used abused by this satsang singer but who cares...
may god bless them
- April 28, 2010 at 3:15 AM
I just spent a few days with Sri Sri and I have a really difficult reconciling what most people post here with the rather nice, spiritual man I interacted with. Perhaps some of your claims have some merit, but the hyperbole comparing him to Hitler, Stalin is really ridiculous. Why don't you have more of a rational discourse instead of all the "screaming"?
- April 29, 2010 at 2:08 PM
@Anon 2:08PM
Nobody is "screaming" here. We are having a very "rational discourse" about what absolute power may do to nice people, when they decide to become owners of the world or Lords of Universe.
"Actually, Hitler before 1918 had been a nice man. There is a volume of evidence that he had liked Jews. Why? He was reading serious books in libraries, being fond of political discussions, painting, dreaming of becoming a great artist, and knowing all of Wagner (and a great deal of Beethoven) by heart. He had been polite, well-mannered, modest, quiet, and avoided all brawls and physical violence...
Having gained absolute power, the nice, gentle, modest young man became absolutely evil. It has been justly said that power corrupts and that absolute power corrupts absolutely. For him, life was now so many precipices, and he could jump into any of them. Do you want to be the owner of the world? Just jump, and you will fly to your ownership of the world – or fall to your suicide."
- April 29, 2010 at 6:03 PM
@Anonymous April 29, 2010 2:08 PM
I am glad you spent a few nice days with SSRS. There are all kinds of perceptions and experiences in this world, whether it's within and outside of AoL.
There is a subjective discussion going on here.
However; the legal systems and social norms of the world define what is ILLEGAL, IMMORAL and UNHEALTHY.
If there is something illegal going on in AoL sanctioned by SSRS - you can continue to have your good experiences with him but authorities can put him in jail.
There are insiders who have left and know first hand, like me, what happens with the money in AOL and a lot of the unethical things. Good you didn't have to face it.
There are many many Crores of rupees that SSRS and his family are sitting on, and there are Swiss bank accounts. SSRS is a very smart, practical, political person back stage. Sometimes he behaves like a shrewd CEO using all the dirty tactics, sometimes like a corrupt politician. Even the heads he's put in place are very close to his own character.
It's like Nithyananda, everything was glorious, the knowledge, techniques, the public image, and then suddenly one day he fell just like that....
- April 29, 2010 at 6:13 PM
- Lehmann108 said...
Again, and again all the hyperbole, but no facts. Just opinions and personal reactions. If you have legitimate claims then make them. Comparing Sri Sri to Hitler is beyond absurd. Some of you seem quite psychologically sound and some of you are a little screwball to say the least.
- May 4, 2010 at 7:11 AM
And why don't you just put your credential on the table & tell everyone you are an AOL PR agent, doing damage control.
Lehmann108 I thought some of you might enjoy this. There is usually kirtan at the end of the talk. I've been practicing his breathing technique called Sudarshan Kriya for close to 20 years now....
Location,Pompano Beach, FLUSA ,(Hometown: Coconut Creek)
- May 4, 2010 at 10:39 PM


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2 Slices Multi-grain Bread
1-2 oz Goat Cheese
1 Ripe Tomato
D'Avolio 18 Year Balsamic Vinegar
D'Avolio Tuscan Olive Oil
Pinch Corse Salt
Heat a heavy skillet on medium.
Thinly slice tomato. Put half the tomato on bread and sprinkle with a little salt. Break up goat cheese on tomato and drizzle a little D'Avolio 18 Year Balsamic Vinegar on top. Cover with remaining tomato slices.
Drizzle D'Avolio Tuscan Olive Oil in pan and place sandwich on oil sliding it around the pan. Cook until brown (a few minutes) on one side and flip. Don't over cook!
Enjoy with fresh peach slices drizzled with the Balsamic Vinegar.


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Mustang MonthlyFeatured Vehicles
1971 Ford Mustang Mach 1
Bruce Wilcox's '71 Mach 1 Has Been Paying Big Dividends For His Farming Family Since High School
Tio Vista, California, is located in the heart of the world's breadbasket-California's Central Valley. Surrounded by neighboring Fairfield, Lodi, Stockton, Hayward, and Sacramento, Rio Vista is the beating ventricle of home-grown commercial agriculture, which has been feeding the globe for more than a century. Bruce Wilcox's family has been farming citrus around the Sacramento River Delta region for generations. He has seen it all over his lifetime-infestations, freezing temperatures, drought, hard economic times, and rolling cycles of gains and losses.
Bruce's Grabber Lime '71 Mach 1 is "High Yield" because it has been paying big dividends since he graduated from high school in 1974. His Mach 1 was a reward for hard work both in school and on the family's farm. Bruce could have purchased a Camaro or Cuda because the market was thick with hot pony cars in those days. But his father wasn't hearing any of it because he had a fierce loyalty to Ford.
That loyalty ultimately saved this car when Bruce bought a Corvette against his father's wishes. Despite the Corvette's arrival, the Mustang remained in the Wilcox family where four brothers drove the wheels off it in the years to follow. In 1988, the Mach 1 went into storage until 2001, when Bruce blew the dust off in a quest to relive his youth.
Of course, Bruce had to ingest some humble pie to get the car back from his father. The grandfather angle helped because Bruce wanted to restore the car for his son, which made it easier for his father to give the car up. Sadly, Bruce's father passed away before the Mustang was completed.
Bruce elected to restore the car as a period restomod from the 1970s, like Bruce remembered. However, it would also be better thanks to today's technology. Bruce wanted handling and safety, which inspired him to fit this family heirloom with Wilwood disc brakes in all four corners. He opted for a Total Control coilover suspension front and rear with Alston Varishocks and five-leaf springs in back. The 15-inch American Torq-Thrust II wheels are wrapped in BFGoodrich Radial T/As. Underneath are subframe connectors to improve chassis stiffness. Shelby underride traction bars sure beat the bolt-on traction enhancers of the period.
Inside, Bruce went the 1970s one better with a Grant steering wheel along with AutoMeter Phantom instruments. Also on board is a Classic Audio sound system with 10-disc CD changer, two 10-inch subwoofers, and a quartet of 51/4- and 4x6-inch speakers.
Under the hood, Bruce had Reddick Brothers rebuild his 351 Cleveland, boring the block to 4.030-inches but staying with the original 3.500-inch stroke. For power and durability, he went with steel I-beam rods, KB forged pistons, Crower cam, 1.73:1 rockers, Edelbrock induction, and aluminum heads. On top is a 750-cfm Holley carburetor protected by K&N filtration. Going with 1970s tradition, Bruce chose long-tube Hedman headers, with newer-style Flowmaster mufflers. In the tunnel is a Tremec five-speed, which offers the efficiency of overdrive. When you spline Bruce's Tremec into a 9-inch Ford axle with 3.89:1 gears, you have a part-time rocket ship and a full-time cruiser.
Bruce's father would be proud. In the end, Bruce returned to the Ford camp with the same hot Mustang he started with, resurrecting a family treasure and winding up with something better and more special than he had 36 years ago.


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STEP Perspective
by Anna Wald, MD(1), Timothy Schacker, MD(2), Lawrence Corey, MD(3)
Infections with herpes simplex viruses (HSV) are very common among persons with HIV infection. Despite the frequent co-infection with both viruses, the interactions between HSV and HIV have been not fully elucidated. However, evidence suggests that these interactions occur on epidemiologic, clinical, and cellular levels:
Genital herpes and transmission and acquisition of HIV
Several studies have found that persons with HIV infection also have high prevalence of HSV-2 infection. However, it remains unclear whether HSV-2 is a marker for high risk sex behavior, or whether it truly facilitates acquisition of HIV infection. Both epidemiologic studies of HIV acquisition and the biology of HSV lesion suggest that the latter is true.
At least five studies conducted in various populations suggest that those with HSV-2 infection are more likely to be HIV infected. The increase in risk of HIV infection ranges from 2-fold to 7.5-fold. For example, in a longitudinal study of heterosexual couples in Europe, those susceptible partners who had a history of genital ulcers were 5.2 times as likely to acquire HIV than the susceptible partners who did not have a history of genital ulcers.
Two biological aspects of genital herpes support the hypothesis that HSV-2 facilitates HIV acquisition. Genital ulcers cause a mucosal disruption, which may allow entry of HIV. Also, genital herpes lesions attract activated CD4 cells that act as target cells for HIV attachment.
Fewer data are available on the relationship between HSV-2 infection and HIV transmission, as transmitters of disease are more difficult to study. However, in an early description of a cluster of HIV infection among women, a man who had HIV infection unknowingly infected 14 of 19 women with whom he had sexual relations. He had a history of recurrent genital herpes.
Other studies have also suggested that transmission of HIV is more likely to occur from a person who has genital ulcers. This has been shown both for female to male as well male to female transmission. In 1989, Kreiss and colleagues detected HIV in 4 of 36 ulcers in women; subsequently, HIV has also been detected in ulcers among men. These early studies were done in Kenya where chancroid was the predominant cause of ulcerations. As genital herpes is the most common cause of genital ulcers in the United States, we have investigated whether we can recover HIV from genital herpes lesions in persons with HIV infection.
Twelve men with a history of genital herpes were enrolled in this study. The median CD4 count was 186 and the median plasma HIV RNA 41,000 (this study was conducted prior to introduction of protease inhibitors). None of the participants had a history of difficult to treat genital herpes. The 12 clients were followed for 26 episodes of genital herpes; 23 healed without anti-herpes therapy, while 3 healed after administration of acyclovir. Clients were seen within 24 hours of new recurrence and then every other day, and swab samples were obtained from their genital lesions for HIV polymerase chain reaction (PCR) assay. HIV RNA was detected in 25 out of 26 recurrences and in 116 of 170 lesion samples. Three-fourths (75%) of the HIV RNA-positive samples contained 10,000 or more copies of HIV/ml. In addition, the PCR signal was detected only when reverse transcriptase was added to the reaction, suggesting that only virion RNA was present and not proviral DNA. HIV was detected in lesions of people with high and low viral loads, and regardless of concurrent antiretroviral therapy. In one person in whom acyclovir was started on the fifth day of his genital herpes recurrence, the levels of HIV RNA in lesions fell rapidly as the lesions healed.
This study supports the hypothesis that persons who have HIV and genital herpes may transmit HIV infection to others more easily than those who are not HSV-2 infected. In addition, it suggests that therapy of genital herpes may curb transmission of HIV to susceptible sexual partners.
High rates of HSV shedding in the genital tract of the HIV infected persons Large, chronic, persistent herpes ulcers were among the first opportunistic infections described in homosexual men in 1981. Since that time, advanced HIV infection has been associated with severe genital herpes and the emergence of acyclovir resistance. Because of the unusual severity of genital herpes in some HIV infected persons, persistent herpetic ulcerations are an AIDS-defining diagnosis. Yet in spite of the anecdotal reports of painful and difficult to treat genital herpes in some persons with HIV infection, the natural history of HSV in HIV infected persons has not been well defined. Clinical experience suggests the rate of clinical recurrences (outbreaks) may be increased and that the response to antiviral therapy may be delayed.
To assess the impact of HIV infection on the natural history of genital herpes, we followed prospectively a cohort of 68 men with HIV and HSV-2 infection. The men obtained daily swabs for viral culture from the urethra, penile skin, and the perianal area, and maintained a diary of recurrences. The median duration of study participation was 55 days. We found that, overall, the rate of shedding was very high: HSV-2 was isolated on 9.7% of days of cultures. In comparison, HIV seronegative men have a significantly lower rate of shedding: 3.3% of days for men who have sex with men (MSM), and 4.7% for heterosexual men in two separate studies. Shedding was especially high in the perianal area, where virus was isolated on 8.6% of the days. Of interest, the most common site of shedding among MSM men who are HIV-negative is also the perianal area (2.9% of days), while among heterosexual men the most common site is the penile skin (3.3% of days). Most of the increase in the total shedding rate is accounted for by a dramatic increase in the subclinical shedding rate, defined as the presence of the virus on skin in the absence of herpes lesions. The subclinical shedding rate was 7.3% of days among HIV-positive MSM, compared with 2.4% of HIV-negative MSM and 2.2% of HIV-negative heterosexual men.
Thus it appears that the viral shedding rate is about three-fold higher in HIV-positive versus HIV-negative men. The shedding rate was especially increased among men who have CD4 counts below 200: the risk of shedding was twice as high among men with CD4 counts less than 200 versus those with higher CD4 counts. Therefore, the increase in the rate of viral shedding appeared closely related to the degree of immunosuppression.
In a smaller group of people, we also examined viral shedding using the HSV DNA polymerase chain reaction (PCR) test. This test was developed at the University of Washington and detects minute amounts HSV DNA (1 to 10 copies/sample). Among 14 men who were studied with both viral culture and HSV DNA PCR test, HSV was isolated in culture on 25% of days, but HSV DNA was detected on 48% of the days. In fact, 5 of 14 men had HSV DNA detected on more than 50% of the days. The high rate of positivity by both culture and PCR was especially striking in men with CD4 counts under 200.
The HSV DNA PCR assay is also able to estimate the number of viral copies present in each sample. Using this semiquantitative measure, we found that people with a CD4 count under 200 had 10 times the HSV DNA in the swab samples than people with higher CD4 counts had. Therefore, it is clear that persons with HIV-induced immunosuppression not only shed HSV more frequently, but also that the shedding is associated with much more virus on the genital skin. HSV reactivation upregulates HIV replication.
Several in-vitro laboratory studies have indicated that certain regulatory HSV proteins (ICPO, ICP27, and VP16) can upregulate HIV replication. In addition, both HSV-2 and HIV can co-infect CD4+ cells suggesting that these viruses may interact frequently in vivo. At the same time, several clinical studies have shown that opportunistic infections, or other means of immune activation (such as Pneumocystis carinii pneumonia, bacterial pneumonia, tuberculosis, or immunizations) can stimulate HIV replication and, at least transiently, increase viral load. Recently, Mole and colleagues have shown that the plasma HIV viral load increases in people with recurrences of genital herpes. It is not known how these increases contribute to overall progression of HIV disease.
Intriguing results have also been obtained from clinical trials that suggested that administration of acyclovir is associated with increased survival in HIV infected persons. While not all of the studies found that effect, there is speculation that reactivation of HSV may accelerate progression of HIV disease.
To examine this issue, we followed 12 people (whose median CD4 count was 246) who were on stable antiretroviral therapy (prior to introduction of protease inhibitors). Clients with serial plasma HIV viral loads were evaluated, initially without acyclovir, and then while being treated with acyclovir 800 mg tid (three times a day). The median period of observation was 65 prior days prior to acyclovir and 62 days on acyclovir therapy. Plasma HIV RNA was determined on average twice a week during these observations. We found that the HIV RNA decreased from a mean of 25,527 to 16,444 copies/ml, a 35% decrease. Also of interest, the decrease was observed in all 12 people. This study supports the observation that acyclovir may slow the progression of HIV disease by preventing reactivation of HSV.
Currently available data suggest that several important interactions occur between HSV and HIV. First, HIV shedding from genital herpes lesions is frequent. Therefore, HSV is likely to facilitate transmission of HIV to uninfected sexual partners. Second, HSV shedding in men with HIV infection is chronic and mostly subclinical. Because men are not aware when they are shedding HSV, they may engage in unsafe sex during HSV reactivation, increasing the risk of transmission of both HSV and HIV. Third, acyclovir therapy appears to decrease plasma HIV RNA. This supports the importance of HSV as an endemic opportunistic infection and suggests that chronic antiherpes therapy may provide benefit in some persons with HIV infection.
These studies leave several questions unanswered:
Any person interested in participation in studies designed to answer these important questions is invited to call the University of Washington Virology Research Clinic at 206-720-4340 for more information.
Timothy Schacker, M.D., Department of Medicine,
University of Washington, Seattle, Washington,
Lawrence Corey, M.D., Departments of Laboratory and Medicine, University of Washington, Program Infectious Diseases, Fred Hutchinson Cancer Research Center, Seattle, Washington
Selected references:
HIV Drug Resistance and the Other Causes of Treatment Failureby Jeffrey T. Schouten MD
The key point to emphasize is that HIV can only become resistant to a drug
if it is actively replicating (reproducing itself). When HIV viral loads
are reported to be "non-detectable," this is very misleading. What a
"non-detectable" result really means is that the amount of HIV present in
the blood is below the limits of the viral load test to detect HIV. Most
clinics in the country use tests which can detect 500 (or more) copies of
HIV, per ml of blood. Thus, "non-detectable" means that you have 499 (or
less) copies of HIV, per ml of blood. These tests are called "sensitive"
viral load tests. There are now several companies which have
"ultra-sensitive" viral load tests available, which can detect 20 (or more)
copies of HIV, per ml of blood. Thus, a "non-detectable" result from such a
test would mean that you have 19 (or less) copies of HIV, per ml of blood.
More accurately, the test result should be reported "below the limits of quantification", not "non-detectable". This is not a trivial point, as will be discussed in this article, the chance of HIV developing drug resistance may be very different if your viral load is 490, versus 0 copies; yet, in both situations the current, most widely-used viral load tests would report the result to be "non-detectable." "You'd better get that drug when it's new, because it won't work as well once it's been around for a while." The factors leading to this truism of medicine will explain many of the issues involved in the recent reports that the new anti-HIV drugs control HIV replication for only about half of all HIV-infected persons.
Reports by researchers from the University of California at San Francisco presented at the ICAAC meeting in Toronto, in September, 1997, showed that 53% of persons at their HIV clinic did not achieve long-term suppression of HIV replication with combination therapy. This contrasts to the controlled trials of highly active antiretroviral therapy (HAART) which showed that triple drug combinations, including a protease inhibitor (PI), completely suppressed HIV replication for 1-2 years in up to 80-90% of persons studied. Why, then, do only half of persons treated in the "real world" achieve a similar result?
Factors Contributing to Treatment Failure
Trial Participation Selection
Clinical trials are very selective in which people they enroll into the trial. "Inclusion criteria" often exclude persons with significant liver, kidney, of blood disorders.
A concrete example of the impact of this selection process is that people with chronic liver disease, such as many HIV-infected injection drug users with chronic hepatitis C infection, often experience worsening of their liver disease when treated with protease inhibitors (PI). Had these people been included in the initial PI trials, the results would not have been so good. Additionally, controlled trials usually enroll persons who are more compliant, more educated, and more motivated to seek out the latest, best treatments. Some of these factors are correlated with better treatment results, than those attained by the broad spectrum of all persons seen in a clinic.
Some trials exclude persons who have been treated with PI's or reverse transcriptase inhibitors in the past. This may be done, for example, by a protocol which offers a new protease inhibitor (PI) to people who have failed all other PI's, but also requires that the person be on two reverse transcriptase inhibitors (RTI) which they have never taken before. If a person has been on (and failed) all the RTI's currently available, then they will not be able to participate in that trial. The fact that a drug performs better in a controlled trial than in the "real world" is not unique to anti-HIV drugs, but it has created inflated expectations of the efficacy of the new anti-HIV drugs in the eye of the public, many health care providers, and people living with HIV.
Due to the unique ability of HIV to mutate, drug resistance can arise when a person misses even a couple of doses of a drug (i.e. "is not compliant"). Thus, if a person is on a combination of drugs which is completely suppressing all HIV replication in their body, resistance to the drug cannot develop. However, if such a person were to miss a few doses of their medication, then some HIV replication may occur, allowing the opportunity for the virus to become resistant to the drugs that person is taking. It has been estimated that the virus makes a mistake once every 10 times that it copies itself. Many of these mistakes result in a defective virus which is unable to infect other cells. However, every so often, one of these random mutations results in the virus being resistant to a specific drug.
So, if the person is taking that drug to which HIV has become resistant, then that particular mutant will grow unchecked and become the dominant virus in the person's system. Because there may be up to a billion copies of HIV in the body, many mutations occur everyday if there is high level of HIV present (a high viral load). Thus, one of the major factors causing treatment failure is mutation of HIV, resulting in HIV not suppressed by a particular drug. This most often occurs due to lack of compliance, but also may be due to cross-resistance from prior drug exposure or infection with a resistant strain of HIV, as will be discussed below.
Drug Absorption
Another factor resulting in treatment failure is inability to absorb the drug that a person is taking. In this situation, even though a drug is being taken properly, it is not getting into the blood at adequate levels to completely suppress HIV replication. Due to the many adverse impacts of HIV and opportunistic infections on the gastrointestinal tract, drug absorption can be a major problem for people with HIV infection. If almost no drug is absorbed into the blood, then HIV replication will go on, but drug-resistant HIV will not develop because there needs to be some drug present for a significant drug-resistant population of HIV to develop. However, if some drug is absorbed, then the HIV may become resistant due to suboptimal drug level.
Thus, in the first case, treatment has failed, but not due to HIV drug resistance, while in the latter scenario, HIV drug resistance has resulted from the treatment failure. It is critical to differentiate these two situations. As will be discussed later, resistance to one drug may cause cross-resistance to other drugs in the same class (i.e. PI's). Therefore, in choosing a second drug, it is critical to know whether or not the reason for treatment failure was due to drug resistance.
Drug Activation
Some drugs are administered in a form which requires the body to change the drug into an active form. This may be done, for example if the active form is not absorbed well or is unstable. This is the case for zidovudine (AZT). The body must convert zidovudine into the active form, before it can inhibit the HIV reverse transcriptase enzyme. If the person's own metabolic activation system is not functioning properly (or is genetically different) for the required metabolic conversion, then the drug will not be effective. As with poor drug absorption, a defect in the activation of the drug could result in very low levels or in higher, but still sub-optimal levels. Thus, you might have treatment failure due to very little active drug in the system or due to drug resistance, resulting from sub-optimal levels of the activated form of the drug.
Drug Metabolism
As with drug activation, there are differences in people's own metabolic processes which remove drugs from the body. The rate of absorption and the rate of drug removal determines how much drug is in a person's system and for how long. This is critical for determining the amount and frequency of a drug to take (in order to achieve optimal blood levels) so that HIV suppression is maximized while toxicity is minimized. The most common methods of drug removal from the body are metabolism and/or inactivation in the liver, and excretion by the kidneys into the urine. For some anti-HIV medications, these are very critical processes.
The long list of drug interactions with ritonavir is due to the changes caused by that drug in liver metabolism. The result is that some drugs are metabolized much slower and thus reach much higher levels in the blood, while other drugs are metabolized much faster and thus attain very low blood levels. For example, saquinavir levels are raised by ritonavir. Thus, the usefulness of combining these two drugs is that much higher and more effective blood levels of saquinavir (which is poorly absorbed) can be attained if it is administered with ritonavir.
Conversely, some drugs may be markedly reduced due to the effect of ritonavir on the liver's metabolic processes. These considerations are important to achieve the desired blood level of an anti-HIV drug. Since the effect may vary from individual to individual, ideally, blood levels of the drugs should be measured to determine if, in fact, the drug is getting into the blood at the desired level. This is what is done in early clinical trials (Phase 1 Trials), but it is not routinely done in clinical practice.
Drug-Drug Interactions
Another reason for treatment failure may be due to the direct interaction of two drugs against HIV. Whenever two drugs are used to attack the same bacteria or virus, there may be one of three interactions. The two drugs may work individually, they may augment each other (synergism), or they may inhibit one another (antagonism). So, with synergism, the sum of the two is greater than the individual effect of each added together, whereas with antagonism, the sum of the two is less than the individual effect of each added together. This is why it is important to test drug combinations in clinical trials, because this interaction is not always predictable. A problem today is that because there are so many FDA-approved anti-HIV drugs, it will take many trials and a lot of time to test a new drug in all the possible three, four or five-drug combinations with the currently FDA-approved drugs. Care should be exercised when combining drugs which have not been combined in prior clinical trails.
HIV Drug Resistance
The most common cause of HIV treatment failure is drug resistance, usually due to a combination of the factors discussed above. However, it is also possible that a person may have HIV which is resistant to a drug they have never taken. This may be due to cross-resistance from another drug in the same class (like another PI) that they have taken, or the strain of HIV that the person was infected with was already resistant to the drug, or the HIV developed resistance prior to any drug exposure by random, spontaneous mutation after infection.
Drug resistant usually develops because HIV undergoes a mutation in its genetic material which allows the virus to reproduce in the presence of adequate levels of the drug. In the case of the nucleoside and non-nucleoside reverse transcriptase inhibitors, the genetic mutation causes a change in the structure of the HIV's reverse transcriptase enzyme, which translates the HIV RNA into the host cell's DNA. The result of the mutation is that transcription occurs, even in the presence of the drug, which had previously prevented this process. Similarly, in the case of the protease inhibitors, the genetic mutation results in a change in the HIV-produced protease enzyme which is necessary for assembly of infectious viruses. Testing for drug resistance may be performed by two methods: genotype and phenotype testing.
Phenotype testing is a functional test whereby the HIV is isolated from a person's blood, is placed into a test tube and grown in the laboratory to test its ability to grow in the presence of a particular antiretroviral drug. This test takes several weeks to conduct and is very expensive.
Genotype testing analyzes the genetic sequence of the HIV when isolated from a person's body. Then mutations in the genetic sequence are looked for, which are known to be associated with HIV resistance to a particular antiretroviral drug. This test costs about $300 and can be done quickly.
Currently, neither test is approved by the FDA, and they are not paid for by private or government insurance programs. There is debate among HIV treatment experts about the usefulness of these tests in the clinical treatment of HIV. Currently, many HIV research programs are studying genotype testing.
Cross Resistance
There is now excellent data to show that when a person becomes resistant to saquinavir, ritonavir or indinavir, they are probably resistant to all three of these protease inhibitors. However, some of the data presented at the ICAAC meeting in Toronto in September, 1997 suggested that resistance to nelfinavir may not cause cross-resistance to the other PI's. Other data has suggested that if a person develops a high level of nelfinavir resistance, they will, in fact, also be resistant to the other three PI's. In theory, a person should select a drug in a class (such as PI's) for front line use which has the least possibility of causing cross resistance. Thus, if a person becomes resistant to that first drug, there are some other options available in that class of drugs. Because PI's, nucleoside reverse transcriptase inhibitors and non-nucleoside reverse transcriptase inhibitors all work at a different point to inhibit HIV replication, there is not cross-resistance between the classes of drugs, but rather it is a problem within a class of drugs.
One potentially beneficial use of genotype testing would be when a person has failed a triple-drug combination, testing could provide useful information in determining which of the three drugs the person has become resistant to so that all three drugs would not necessarily have to be abandoned. Mutations identified by genotype testing are reported by the location in the genetic sequence of the virus where the change has occurred (the codon). There are a series of known changes in the genetic sequence of HIV which are associated with resistance in the clinical situation. So, a report might note mutations at codons 41, 67, 70, and 215. These are all sites known to result in resistance to zidovudine.
There are some serious limitations to genotype testing for drug resistance. Drugs such as ddI and d4T do not show genetic mutations which correlate as clearly with clinical resistance as does zidovudine. The genetic change seen which confers resistance to 3TC may actually be beneficial in that the particular genetic change in HIV associated with 3TC resistance confers increased sensitivity to zidovudine (i.e. it makes HIV more likely to be inhibited by zidovudine). With some drugs, only one or two mutations are necessary to make HIV resistant, while other drugs (such as zidovudine and saquinavir) may require several mutations in HIV to confer complete resistance to these drugs (although one mutation at codon 215 will cause complete resistance to zidovudine). Unfortunately, a report of genotype testing does not give a simple answer to which drugs to use. If that were the case, there would be a stronger call to make the test available to all people living with HIV and for government and private insurers to pay for it.
A major limitation of genotype testing is that you need to get a sample of HIV from the patient's blood, and if the viral load is very low this may be difficult. Additionally, there exist in the blood several different populations of HIV, so that some, but not all, of the HIV in your body may be resistant to a drug, but the test may not accurately sample that subpopulation of HIV. The test does not report the number of HIV which contain a specific mutation; it is not a quantitative test. There is a concern that drugs which may be beneficial to a person would be discontinued prematurely (since the presence of a mutation does not mean that the drug is 100% ineffective); or, conversely, drugs which are not helping a person might be continued based on a misleading genotype report showing no mutations present.
Another use for genotype testing for resistance might be prior to initiating any anti-HIV therapy, either in a person recently infected, or someone who has been infected for a long time. One study, reported at the 4th Annual Conference on Retroviruses and Opportunistic Infections, in January, 1997, revealed that in a rural Iowa population, 26% of persons never treated with a protease inhibitor had some genetic mutations associated with resistance to all three of the protease inhibitors which were then approved, and 3% of newly-infected persons had resistance to some reverse transcriptase inhibitors. Other studies have shown that resistance occurs more frequently with lower CD4 counts, and higher viral loads. It appears that the later therapy is begun, the less likely you are to obtain complete viral suppress, allowing for resistance to develop. Thus, the immune system may help in the prevention of drug resistance. This is another observation in support of the , "Hit hard, hit early" approach.
The most comprehensive discussion of HIV drug resistance can be found in the report issued following the International Workshop on HIV Drug Resistance, Treatment Strategies and Eradication, held in St., Petersburg, Florida, June 25-28, 1997. (The summary and other reports are available on the World Wide Web at: http://www.healthcg.com/hiv/hivresistance/content.html.) The main findings were: the realization of generalized resistance across the class of protease inhibitors (cross-resistance), (although as noted above, whether this applies to nelfinavir is not known at this time) highly active antiretroviral therapy (HAART) can suppress viral load levels to very low levels to minimize the chance of resistance developing, even in persons with very low CD4 counts, as long as they were not treated with a lot of antiretrovirals in the past; resistance assays need to be developed to tell us which drugs to use, but at this time, we do not know how to interpret the data; and, antiretroviral therapy needs to be individualized. This report lists, in tabular form, all the known genetic mutations associated with resistance for all the currently available antiretroviral drugs.
One other point emphasized is that once you become resistant to a drug, even if you are off of that drug for one year or longer, the resistant virus is still present and repeat use of that drug will be unsuccessful.
ConclusionThere are many factors which can lead to HIV treatment failure. The most important is the development of resistance to the antiretroviral drug (or drugs). The two most important factors to consider are the amount and nature of prior therapy and compliance with a difficult treatment schedule. An inexpensive, accurate laboratory test which can tell which drug is going to work in an individual person would be very helpful in designing treatment plans. The current genotype and phenotype tests do not yet accomplish this goal. However, for some people, a genotype test may be useful to select antiretroviral drugs, particularly when that person has been treated with many antiretroviral drugs in the past.
What's New in Kaposi's Sarcoma Research
Kaposi's sarcoma (KS) is a cancer of cells lining blood vessels and is commonly seen as a complication of HIV infection. Prior to the HIV era, KS was rarely seen, and when it was seen, it seemed to favor males over 50 years of age who were of Mediterranean or African origin. Otherwise healthy women and children were rarely affected by KS. Since the beginning of the AIDS epidemic, KS has been seen primarily in gay men with HIV infection. KS is also seen in people who have received organ transplants, due to the use of drugs that suppress their immune response to the transplanted organ.
Recently, Chang and Moore found sequences of viral DNA in KS lesions (1). This viral DNA was found to belong to new virus belonging to the herpesvirus family. Several investigators have found human herpesvirus-8 (HHV-8) DNA in almost all KS lesions examined (2-5). Other more common viral DNA has also been found in KS lesions; however, no other virus appears as consistently as HHV-8.
It is clear that HHV-8 DNA is consistently found in KS lesions and recent studies report finding HHV-8 DNA in saliva, certain white blood cells (B-lymphocytes), semen, prostate tissue, fecal material, and occasionally in normal skin of people with KS (6-8). However, not all of these reports have been confirmed by other investigators, so that controversy remains regarding the prevalence of HHV-8 at various sites.
There are two reports from investigators who have been able to grow infectious HHV-8 virus from KS lesions (Foreman) and from white blood cells (Blackbourn) of a healthy blood donor (9, 10). These findings suggest HHV-8 can be transmitted through contact with infected secretions. However, the exact mode of transmission and the efficacy of transmission of HHV-8 remain unknown.
HHV-8 is likely to be transmitted via sexual contact. While some epidemiological studies suggest that oral-anal contact may be a risk factor for development of KS (11), such contact would not be expected to be a strong risk factor for transmission of a herpesvirus. Therefore, these findings must be interpreted cautiously. Other risk factors for KS include past history of having an sexually-transmitted disease (STD) other than HIV, a high number of casual sex partners, and a high frequency of sex acts. A report from McCarthy details the case of an HIV-positive mother and vertically (at birth) HIV-infected child who both developed KS (12). This is further support for transmission via infected secretions or blood.
There are numerous reports of HHV-8 DNA recovery from circulating white blood cells and one report of viable HHV-8 recovery from blood. There are no reports of HHV-8 DNA recovery or of seroconversion (acquisition of HHV-8 antibody) after receiving blood products. And, it has been shown that those people who become HIV-positive from blood product receipt (e.g., hemophiliacs) are very unlikely to show evidence of HHV-8 infection. However, it remains unknown if blood and/or blood products can transmit HHV-8. Blood tests for HHV-8 antibodies have been developed and are available in some research laboratories. The sensitivity and specificity of these tests are under study and newer methods to detect HHV-8 infection are also under development.
The prevalence of HHV-8 seropositivity (presence of the antibody that indicates infection) in different groups has been examined. It appears that HHV-8 seropositivity is greatest (80%) in HIV-positive gay men with KS. HHV-8 seropositivity is 18% in HIV-positive/KS-negative gay males. In contrast, among HIV-positive hemophiliacs and HIV-negative healthy blood donors, none had antibody to HHV-8 (13). Among people presenting to the STD clinic with a positive serologic test for syphilis, 13% had antibody to HHV-8 (14).
The strongest evidence for causal role of HHV-8 in the pathogenesis of KS is the temporal association between seroconversion to HHV-8 and the development of KS. In a study of 40 men with HIV and KS, 52% had seroconverted to HHV-8 a median of 33 months prior to development of KS.
While the association between HHV-8 infection, immunosuppression, and subsequent development of KS appears strong, much more work needs to be done on HHV-8 epidemiology to gain a clear definition of risk transmission. Thereafter, strategies can be recommended.
Laboratory studies suggest that HHV-8 is susceptible to ganciclovir, foscarnet, and cidofovir, and resistant to acyclovir (14). It is unclear if antiviral treatment of HHV-8 infection prior to KS onset can prevent KS or eliminate HHV-8 carriage. The latter seems unlikely, as all other herpesviruses establish life-long latency in the human host. In addition, available effective antivirals can cause significant toxicity and their use as KS prophylaxis may not be appropriate.
The treatment of established KS varies from no treatment to systemic multi-drug chemotherapy. Liquid nitrogen has been used on small isolated lesions and local radiation therapy has been used to treat diffuse lesions of the lower extremities. Topical retinoids (vitamin A compounds) are showing promise and are likely to be approved for use soon. In non-HIV immunosuppressed people, withdrawal of some or all of the immunosuppressive drugs sometimes results in clearance of KS. More often, systemic chemotherapy is required and many times response to therapy is incomplete (15).
Even when complete clearance is achieved, later recurrence is not uncommon in all forms of KS. It is unknown if long-term clearance of KS could be achieved by antiviral treatment and suppression of HHV-8 infection. Co-treatment of HHV-8 infection and KS is likely to be studied in the future. There is little information on the relationship between the quantity of HHV-8 DNA in blood (and perhaps tumor) and response to treatment.
The relationship, if any, between HHV-8, DNA quantity, and treatment response needs further study. Intra-lesional human chorionic gonadotropin (hCG) has been shown to induce KS regression in ten of 12 human KS lesions; HHV-8 DNA levels were not reported. Interferon alpha-2a has also shown promise in treating KS. Much progress has been made in understanding the etiology and pathophysiology of KS. As our research progresses and our understanding of HHV-8-KS increases, better treatment will evolve. The University of Washington has an active research program investigating the basic science, clinical and epidemiological aspects of HHV-8 infection. An antibody test for HHV-8 has been developed for research purposes.
The Virology Research Clinic can be contacted at (206)720-4340.
Virology Research Clinic
1001 Broadway, Suite 320
Seattle, Washington 98122
(206)720-4371 fax
References cited:
Primary Infection Clinic Enrolling for NIH Studiesby Michelle Berrey
The Primary Infection Clinic began in September of 1992 with the goal of following the natural history of early/acute HIV, an area about which very little was known at the time.
In the past 5 years, partly as a result of our work, knowledge surrounding acute or primary HIV has grown from a suspicion about a viral conversion syndrome to a well-described clinical symptom complex of pharyngitis, fever, and fatigue (1).
The variation of symptoms and severity of illness among individuals is marked, and may range from a mild sore throat that lasts only a couple of days, to high fevers, rash, and headache that require hospitalization. The most common symptoms reported in our natural history study at the University of Washington are fever and/or night sweats, sore throat, headaches, muscle aches (similar to those experienced with the flu), fatigue, and rash.
Dr. Phillipe Vanhems of France recently compared our data to two primary infection clinics in Geneva, Switzerland and Sydney, Australia. He found reassuring evidence that the same symptoms we see here in individuals seroconverting were seen in both Australia and Switzerland. Other symptoms seen less frequently in all three clinics were oral and genital ulcers, swollen lymph nodes, diarrhea, and anorexia (loss of appetite).
Our recent data suggest that individuals with more severe syndromes, i.e., those who present to medical attention, may have a more rapid progression to clinical AIDS (2), suggesting a strong need to identify all such cases early and to offer early treatment. Local HIV/AIDS epidemiologists in the State Department of Health and the Seattle-King County Department of Public Health estimate that we continue to have 600 to 900 seroconversions per year in this state, possibly half of which have a symptomatic seroconversion syndrome (3).
We know from our data that only about half of persons with HIV who present to their medical provider with symptoms will be screened for HIV antibody. We hope that reminding the public and providers about primary HIV will increase the number of infections caught early on. Symptoms are not required for enrollment in the Primary Infection Clinic, however. I have outlined our criteria below, but we are happy to perform all screening bloodwork.
After an initial behavioral-risk-factor interview, consent forms are signed to allow blood to be studied for antibody, viral load testing (plasma RNA), proviral HIV detection (DNA PCR), CD4+ cell count, and cellular response to the potential HIV infection (cytotoxic T-lymphocytes). During very early HIV infection, the anti-HIV antibody (the antibody that is detected on the standard screening test) may remain negative for 6 weeks after the infecting exposure, so it is important to test for HIV RNA in the plasma, which may be detectable within 10 days after exposure. It takes a week to get the viral load (RNA) back from the lab; at that time we review the results and discuss potential studies for enrollment, which I discuss below.
Our contribution to the current understanding of early HIV infection has recently been recognized with a 4-year, multi-site, $6.7 million/year grant from the National Institute of Allergy and Infectious Diseases for the continuation of our studies. The Aaron Diamond AIDS Research Center, the University of California at San Francisco, Johns Hopkins University School of Medicine, the University of Colorado Health Sciences Center, and the University of Alabama at Birmingham will be collaborating with us on the Acute Infection and Early Disease Research Program. We have established a cooperative network with clinics in Minnesota (Tim Schacker); Cincinnati (Judith Feinberg); National Institute of Health (Anthony Fauci); Sydney, Australia (David Cooper); and Geneva, Switzerland (Luc Perrin) to better understand the evolution of the infecting virus, the cellular immune response of the host (particularly the early defect in immune response), emergence of the neutralizing antibodies, and how pharmaceutical intervention may impact all of these.
Who can be enrolled?
What studies are being offered?
The Primary Infection Clinic's natural history study enrolls individuals who meet the above-listed criteria to better define the clinical, virologic, and immunologic characteristics of primary HIV. The study provides free laboratory tests including viral load testing and CD4 counts, and offers optional testing of semen viral load and lymph node biopsies. The study is ongoing and is not limited to a maximum number of participants.
We are currently enrolling in a trial of "triple" drugs: AZT (zidovudine), 3TC (lamivudine), and indinavir (Crixivan) to study the effects of early intervention on the mutations of the virus, the viral replication rates, CD4+ cell counts, and other measures of immune system integrity. The study provides free medication for 12 months, as well as free lab tests during the study. The study is limited to persons infected within the last 3 months (with a recent negative EIA or with symptoms suggestive of recent infection), and will include a maximum of 10 enrollees.
The International Acute Infection and Early Research Network grant funded by the NIH will also include a pharmaceutical intervention with multiple antiretrovirals. This trial will begin enrollment around the first of 1998. Medications will be provided, as will frequent lab monitoring.
Drug treatment during primary HIV has the theoretical benefit of attacking HIV when the virus has perhaps not established a foothold in the body, when the immune system is strongest, and while a relatively homogeneous strain of virus still predominates. However, there is also real concern that we may be using up our "magic bullet" too soon -- that over the long haul early therapy will not always be optimal. And, of course, there are toxicities with all these drugs.
The trials performed in our clinic are designed to observe clinical as well as viral and immunologic parameters in early intervention, and will, we hope, reveal some of the predictors that may help us be able to decide very early whether someone would benefit from very early intervention, or whether his or her own immune system will be able to control the virus.
To answer questions means we need to see people and enter them into clinical trials. Our approach is to allow individuals to select their therapeutic approach with their primary care providers, although we are certainly available at any time to help with therapeutic decision-making. Through the new Madison Clinic at Harborview we can also provide primary care for those people who do not have a regular provider.
Please feel free to contact us at any time with questions at 206-667-5300, or toll-free within the state of Washington at 800-968-1437.
You can also reach the clinic via e-mail at firstname.lastname@example.com.
Although we hope for the fewest possible seroconversions, it is our hope to have every case of early HIV identified and referred to us.


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Benjamin P. Tu, Ph.D., associate professor of biochemistry at UT Southwestern Medical Center, was honored on March 27 with the 2014 Norman Hackerman Award in Chemical Research. Tu was recognized for innovative studies of once-unappreciated molecules that may someday improve treatments for cancer or conditions associated with aging.
The award is given by the Houston-based Welch Foundation, one of the nation's oldest and largest sources of private funding for basic research in chemistry. The Welch Foundation presents the $100,000 award annually to honor early career scientists at Texas institutions who are expanding the frontiers of chemistry.
Read the news at www.utsouthwestern.edu.
Watch a brief video about Dr. Tu's work:


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Nice twist to the known game.. Although to run it can be a catch for newer macs. Before clicking 'cider' you have to downgrade the resolution at least to 1280x720. Have fun!
May be you can think is more of the same, but it is really a nice Bioschock sequel. Great graphics, better soundtrack and a good gameplay; better if you get it with discount though.
Although in easy mode it can be too short. it is a great story with nice graphics and cinematics. It would be great to have an expansion or another sequel.
If this a game to reccomend. For all fairness, this was the first game of the saga i play. May be better to star from the begiging.
A nice kind of retro shooter with a twist in improving the character thru the game. Reccomended on sale.
Although there is a sequel to this game, this should be the final season. Very nice development of the story line, great soundtrack.
Got stuck on the game, hope can understand how it works.. the keyboard doesnt respond as should in some part.
Very nice part II for Bioshock Infinite... Enjoy it all the way!
Yes! a very fine game, with very nice scenarios and plot. It was my first Bioshock and Im glad I waited to play it.
Come with the Starter Package.. haven't really payed it attention.
Very nice Ep.2 for Bioshock Infinite:Burial at the Sea..
This chapter is in between seasson one and two.. although I though the story line was going to be longer, it was good enough.
Im a fan of Telltale, so I knew was going to be funny and entertaining. I unloked all hours ago but cant stop playing. It would be great if Telltale upload pacthces for changing the characters conversation.
Great story line where you will have to make some hard choices. Difficult to not make emphaty with the characters. Totally recommended! Im starting the 400 days and have the second seasson waiting.. see ya!
Another great game by Telltale.. I also hpe there is a Sequel.


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Elijah Parish Lovejoy (1802-1837) was a Presbyterian minister in St. Louis, Missouri. He began publishing a religious newspaper, The St. Louis Observer, and advocating the abolition of slavery. He moved to Alton, Illinois, in July, 1836 after his press was attacked by a mob. He actively supported the Anti-Slavery Society of Illinois, which enraged many of the citizens. Even after three presses had been destroyed, he continued to publish the Alton Observer. On November 7, 1837, a mob attacked the warehouse where a new press was being stored, and Lovejoy was killed. This article reports on a meeting to be held in Shelburne in response to this episode which helped galvanize the anti-slavery movement. The Gazette & Mercury was the newspaper in Greenfield, Massachusetts, from June 27, 1837 to July 13, 1841, when it changed its name to the Gazette & Courier.
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Pages from the diary of Martha Cochran
"County Anti-Slavery Meeting" article from Gazette and Mercury newspaper
"The American Anti-Slavery Almanac for 1838"
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Ford 350/450 shifting advice
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Ford 350/450 shifting advice
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OwnPC: Yes
NewUsed: Used
PurchDate: September 2013
Model: 2350 Ford
ModelYear: 2013
Slide: Yes
Location: Oklahoma City
Ford 350/450 shifting advice
July 16, 2014, 05:36:54 pm »
I am curious about others experience with the Ford vehicles when in mountains. Our 2350 is pulling a Jeep Cherokee which weighs about 4044 curb pounds. I am surprised how the V10 seems to really pull down on mountain passes, granted they are Rocky Mountain passes where I have experienced this and I am towing. After one trip in June (and planning another in August) we will probably just unhook the Jeep and my wife will drive it up the passes. We will be boondocking above 10,000 feet so I am not talking hills
Here is my question. Do most PC owners use the tow/haul mode which, as I understand it, just changes the shifting points, or do they not use it and just use the downshift from the standard drive position, as well as engine speed to maintain momentum. Our last Class C was a 450 and this is a 350 and we were not towing. I was down to 25 mph going up Bobcat Pass in Northern New Mexico last month. Maybe that is just the way it is? Our most previous RV was a Roadtrek Class B 210 with the Chevy 6.0L
ALSO...I have read in some places that the V10 is designed to develop max torgue at 4500-5000 rpms. Is that correct? I read on another forum a discussion that indicated that was no problem, but I always hate to "cram" an engine.
Any experiences, direction or suggestions you could give me would be appreciated.
OwnPC: Yes
NewUsed: New
PurchDate: 10/17/11
Model: 2551
ModelYear: 2012
Slide: Yes
IntColor: Cherry
ExtColor: Classic Umber
Location: Michigan
Re: Ford 350/450 shifting advice
Reply #1 on:
July 16, 2014, 07:02:32 pm »
We took our 2008 2350 through the Rockies in 2010. We were towing a 2500 pound car and were able to top Vale Pass at around 55 MPH. I never use the tow/haul mode.
One thing I learned about driving in the mountains is to keep your speed up. Don't wait for a downshift before applying additional throttle. Once you lose your speed it is hard to get it back.
Perhaps a more experienced mountain driver can provide addition information on how to approach some long grades.
Barry and Sue
Current 2012 2551 w/Slide
Previous 2008 2350 w/Slide
Ron Dittmer
Ron and Irene
OwnPC: Yes
NewUsed: New
PurchDate: June 2007
Model: 2350 Ford
ModelYear: 2007
Slide: No
IntColor: Cherry Green&Gray
ExtColor: Full Body Gray
Location: Illinois
Re: Ford 350/450 shifting advice
Reply #2 on:
July 17, 2014, 07:01:44 am »
With our 2007 E350-V10 & current day Torqshift transmission, towing our 4200 pound Jeep Liberty, I have yet to be worried over the drivetrain except when engine braking. The RPMs can sometimes get very close to red-line. At my second oil change I switched to full synthetic oil in hopes to provide a little extra edge to my concerns.
Whether engine braking or climbing, the Triton series engine, V10 or V8, is designed to rev very high compared to the GM engines. As a result, the engines can get loud which can make you feel you are over-stressing something. But in reality, all is well.
I personally love the tow haul mode. I called Ford twice over the years, asking if Tow-Haul could be reprogramed to be "On" by default, but I get the same disappointing answer.
As Barry said, try not to loose momentum when driving in the mountains. When you do, just take it slow (or slower) in a lower gear. You want the rig to rev high with the least amount of throttle. Once in a great while you will simply find yourself at very high RPMs in a very low gear, going very slow. As uncomfortable as it might feel, the drivetrain is designed to work just like that. As always, give consideration to the other drivers around you.
In answer to your Tow-Haul mode question... It changes the shift points under both conditions, accelerating and decelerating.
Last Edit: July 17, 2014, 11:29:11 pm by ron.dittmer
Ron (& Irene) Dittmer
Re: Ford 350/450 shifting advice
Reply #3 on:
July 24, 2014, 09:36:55 am »
We aren't experienced mountain drivers (well, in an RV that is), but did have the opportunity to tackle a few mountains on our recent trip coast to coast.
We have a 2552 and tow a heavy Ford Edge (4500+ lbs), both loaded typically for long trips. This is the first trip I've used tow/haul mode and only used it when there was either a series of upcoming ascents/descents or one long or steep ascent/descent. I was impressed by how it functioned, and was especially glad I had it going down a very very steep and windy section coming out of Yellowstone. Never had much of a problem with long, steep ascents if I was able to get the speed up beforehand. But even when I was 'trapped' behind slow moving big rigs I managed 40 mph at about 4300 rpm.....and sometimes was even able to gain speed and pass other rigs, albeit slowly, while on the grade. If you are familiar with grades such as between Cheyenne and Laramie on I-80, or going over the Donner Pass on I-80 (either direction), then this is the type of grade I'm referring to.
I am very happy we have tow/haul!
- Mike
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IntColor: Desert Sand-Hickory
ExtColor: Desert Sand-Lower
Location: Kansas
Re: Ford 350/450 shifting advice
Reply #4 on:
August 29, 2014, 04:10:01 pm »
Having had several years worth of experience with 2 F series Ford chassis cabs, 450's, heavily loaded constantly, 10k+ pounds, in Fire Dept. service, standard operating procedure, and Ford fleet sales recommended, is for us to run them in tow/haul all the time. It's easier on the engine, brakes and transmission.
We have had zero issues with the drivetrain doing this
Bob & Sharon
Current: 2013 Winnebago ERA Class B Sprinter Van
Future: 2100 special, 2350, ?? on a hopefully Ford Transit 350 or 450
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by Joe Tressa
The Friends of the Wissahickon are seeking volunteers to help complete construction work on a new stone staircase recently installed at Kitchen's Lane in Wissahickon Valley Park. The FOW is also working on the Upper Valley Green Parking Lot.
The first phase of construction on the parking lot is scheduled to be completed by Sept. 30. The parking lot will remain closed during the length of this project.
The dates for the second phase of construction are yet to be determined. Visitors of the park are urged to walk, bike, or use public transportation to get to the park.
The project will attempt to improve the water quality in the Wissahickon Creek. It will also improve parking conditions and restore native vegetation. The first phase involves stabilizing the stream bank along the parking lot, while the second phase involves resurfacing the parking lot.
The three upcoming dates when volunteers are needed in the Kitchens Lane area are July 31, Aug. 3 and Aug. 10. The times for all three dates are 9 a.m. to 1 p.m.
To volunteer, contact FOW Volunteer Coordinator Eric Falk at email@example.com or 215-247-0417 x107. Registration is not required, but is recommended in order to be notified in the event of any changes due to weather. Volunteers are encouraged to bike, hike, or carpool to workdays. Workdays will be cancelled in the event of heavy rain. Visit FOW's Facebook page or www.fow.org for updates.


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Edd wrote:Ubi Dubium wrote:black bart wrote:An understandable addiction...went to the Dr Who exhibition recently and bought an inflatable dalek.
I want a full-size weeping angel for my yard! How big is your Dalek?
It's not the size of your Dalek that matters, but how you use it.
Lol... and where you inflate it (it's about 4 ft high).


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Seven reasons Sharks have surged to 7-0 startby Dan Rosen
Patrick Marleau leads the NHL with nine goals and Joe Thornton has a League-best 11 assists, so it stands to reason that the San Jose Sharks would be the best team in the NHL at 7-0-0.
It's not that simple.
If the Sharks only were about Marleau and Thornton, they probably wouldn't be only the 11th team in NHL history to start 7-0-0. Teams don't go 7-for-7 to start a season based on the production of just two players.
There has to be more to this Sharks team, more to this remarkable start, the best in franchise history.
There is.
Outside of Marleau and Thornton, here are seven other reasons the Sharks are 7-0-0:
Joe Pavelski's presence on the top line
While Marleau and Thornton are generating the headlines with their combined 28 points, don't discount what Pavelski has done to help those two get to the top of the leaderboard this season.
Pavelski has acquitted himself quite nicely as the third man on the Sharks' top line with four goals and eight assists. He's scored all four of his goals in the past three games, taking over the scoring load for Marleau, who has gone two straight games without a goal after scoring nine in the first five. Pavelski is the only Sharks player with a point in every game.
The thing with Pavelski is it's not just about offense; it's about faceoffs (59.7 percent), ice time (19:13 per game, most on the team among forwards) and penalty killing (2:21 of shorthanded ice time per game, most on the team among forwards).
If Marleau and Thornton are the Sharks' superstars, then Pavelski is the glue that keeps them together.
2. Defense and goaltending
Again, the headlines coming out of San Jose have to do with offense, mainly because the Sharks are scoring 3.86 goals per game and have a power play that has clicked for a 30.8-percent success rate. However, San Jose's defense and goaltending have as much to do with the 7-0-0 start as Marleau, Thornton, Pavelski and Co.
The Sharks are tied with the Ottawa Senators for the NHL's best defense (1.71 goals-against per game).
Antti Niemi has a 1.95 goals-against average, making him one of six goalies who have started four or more games to carry a sub-2.00 GAA. He also has a .933 save percentage. But don't forget that Niemi's backup, Thomas Greiss, made 24 saves in a 4-0 shutout of the Colorado Avalanche in his lone appearance this season.
Hartnell: Foot injury came earlierBy Adam Kimelman - NHL.com Deputy Managing Editor
Scott Hartnell's foot was actually broken earlier in the game Jan. 22, but he continued to play before getting hit in the same spot again. READ MORE ›
Even more remarkable in all of this is the Sharks are doing it without one of their top blueliners. Brent Burns hasn't played this season and the team has given no definitive timetable for when he'll return from a lower-body injury.
Undrafted 25-year-old rookie Matt Irwin has stepped up in the absence of Burns (and Jason Demers) and has a goal and an assist while playing more than 19 minutes per game, including two minutes per game on the power play.
3. Winning the draw
Simply put, the Sharks are getting a lot of offense because they have the puck a lot of the time.
Why is that? They're winning a lot of faceoffs.
The Sharks are second in the NHL with a 58.5-percent success rate on draws. They're winning faceoffs, keeping the puck and generating offense. There really is no simpler way to put it.
All four of the Sharks' top faceoff guys (Pavelski, Thornton, Logan Couture and Michal Handzus) are better than 57 percent. Scott Gomez has won 68 percent of his draws (17 of 25) since entering the lineup four games ago.
4. Hot starts
The Sharks are outscoring the opposition 12-2 in the first period and have scored four times within the first 4:30 of a game. They haven't given up a first-period goal in the past five games, since Edmonton Oilers rookie Nail Yakupov scored in what turned into a 6-1 first-period rout by the Sharks on Jan. 22.
With their defense, goaltending and ability to win faceoffs, early leads are making the Sharks impossible to beat over a full 60 minutes.
The Phoenix Coyotes and Anaheim Ducks are the only teams that have erased early deficits against San Jose. The Sharks still were able to beat the Coyotes 5-3, coming back from two goals down. They rallied to beat the Ducks 3-2 in a shootout.
5. Quick strikes
In six of their seven wins, the Sharks have sent a dagger through their opponent by scoring multiple goals in a matter of minutes -- sometimes seconds.
There are few things harder for a team to overcome than giving up a couple of quick goals in a row.
Marleau and Martin Havlat combined for three goals in a span of 4:18 of the second period to lift San Jose to a 4-1 win against the Calgary Flames in the season opener. The Sharks scored six times in the first period against Edmonton, including three sets of back-to-back goals separated by 73 seconds, 65 seconds and 71 seconds, respectively.
2012-2013 Standings
San Jose came back to beat Phoenix by scoring three times in the final 10:45 of the third period.
Marleau scored twice in a span of 78 seconds in the first period of the Sharks' 4-0 win against the Avalanche. Similarly, the Sharks jumped all over the Vancouver Canucks with goals by Thornton and Pavelski in the first 3:26 of the first period en route to a 4-1 win.
Couture and Pavelski got the Sharks a 2-0 cushion against Edmonton with unassisted goals 39 seconds apart in the second period.
6. Handzus' shootout supremacy
The Sharks had to go to the shootout to win their past two games, against Anaheim and Edmonton. It's a good thing coach Todd McLellan has Handzus as his leadoff shooter.
Handzus, who still doesn't have a point this season in regulation and overtime, is 2-for-2 in the shootout, and he used the same move to beat Anaheim's Jonas Hiller and Edmonton's Devan Dubnyk -- he came down the middle, made a quick move to fake low, getting the goalie to bite, then shot high into the left side of the net.
Handzus is 18-for-34 for his career in the shootout, and 7-for-12 with the Sharks.
7. Couture provides depth
Couture is as much of a difference-maker for the Sharks as Marleau and Thornton. The opposition can't load up to try to stop the Sharks' top line because coming right behind them is Couture, a back-to-back 30-goal scorer who has five goals and five assists this season.
The Sharks' second-line center, who would be a first-line center on a lot of teams, is just like Pavelski in that he plays on the power play and the penalty kill; he just doesn't play as much.


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DimpleClip necesitaba un nuevo diseño de impreso o envases y lanzó un concurso de diseño en 99designs.
Un ganador ha sido elegido entre 82 diseños de 10 diseñadores freelance.
Dimple Clip
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Dimple Clip is a molded plastic clip designed to sit inside the knot of a necktie to create a dimple in the fabric of a necktie.
It is placed on the necktie just beneath the knot after the knot is tied and slipped up inside to be concealed by the knot, and to ensure the dimple is held in place.
To see our previous packaging, instructions and prior web layout visit http://www.simpleTIEdimple.com
We would like to keep a similar box style, but redesign the logo and graphics printed on the box ... color scheme may also change
Open to new box designs!
Design us a new package that holds three "Dimple Clips" seen in attached photo number 105, measurements included
Current product name is Simple Tie Dimple and we are changing our name and design.
Our New Product Name - Dimple Clip
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Design us a new package that holds three "Dimple Clips" seen in attached photo number 105, measurements included


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Carolina wins two medals, sets six school records on the week
COLLEGE STATION, Texas Feb. 23, 2013 — The South Carolina swimming and diving teams posted four more NCAA provisional qualifying times and swam seven lifetime bests on Saturday night to wrap up competition at the 2013 SEC Championships.
The Carolina men finished the week in eighth place with a total of 540.5, which was in improvement of two spots based on the overall standings from last year. On the women's side, the Gamecocks finished 11th with a total of 248. South Carolina won two medals, broke six school records and swam two NCAA automatic qualifying times during the five days of competition.
"I think for the men's team it's one of the best meets we've ever had," South Carolina head coach McGee Moody said. "We had some outstanding swims and outstanding races throughout the week. The guys battled the entire time. We moved up from our position last year as far as team standings. We could possibly have as many as seven guys go to the NCAA Championships. That's huge for us. We've never had more than two go to a single meet since I've been here.
"In the women's meet, it was kind of a tale of two meets. It was a struggle at the beginning. They had a hard time, and it was tough for them because they weren't performing up the level they expected. Today they finished strong and had very strong races. All in all I think it was a very successful meet for our program."
In the Gamecocks' only championship final race of the night, junior Amanda Rutqvist finished eighth with a time of 2:11.66, scoring 22 points for the team. It was Rutqvist's third straight appearance in the 200 breaststroke championship final. In the men's 200 breaststroke B final, junior Matt Navata delivered an impressive swim, finishing sixth in the final (14th overall) with a NCAA B cut and lifetime best of 1:58.53, which ranks 2nd all-time at South Carolina. Sophomore Alex Vance finished 23rd overall as he touched the wall eighth in the C final with a time of 2:02.67.
In the men's 100 freestyle B final, junior Alex Fitton swam a 44.41 to finish eighth (16th overall), earning 11 points for the Gamecocks.
Freshman Marwan El Kamash gave the Gamecocks a solid start to the night as he scored 11 points by finishing 16th in the 1,650 freestyle with a NCAA provisional qualifying time of 15:19.58, which is the third fastest time in school history. Fellow freshman Alex Eiden just missed scoring with a 25th-place showing. He turned in the fifth fastest time in program history with a NCAA B cut of 15:29.57. In the women's 1,650 freestyle, seniors Whitney Avers (22nd, 17:00.28 PR) and Jordan Gibbs (24th, 17:05.07) scored in their final race as Gamecocks.
In the final event of the night, the Gamecock men's 400 freestyle relay team of Michael Flach, Jay Warner, Gerard Rodriguez and Fitton placed ninth with a time of 2:56.71, the second fastest mark all-time at South Carolina. The Carolina women's team of Lauren Raczkowski, Sara Drake, Caroline Bixler and Rachael Schaffer finished 12th with a time of 3:25.69.
Earlier in the day during the preliminaries, the Gamecock divers concluded another successful SEC Championships. Sophomore Cole Miller made a run at advancing to the finals of the men's platform diving for a second straight year but he came up just short, finishing 10th with a NCAA Zone qualifying mark of 321.70 to score 17 points for the team. Miller was 24.35 points shy of cracking the top eight. Junior Andrew Helmich had a career-best finish of 23rd with a total of 231.30, which is also a career high.
"I was happy with both of them," South Carolina head diving coach Todd Sherritt said. "Obviously, having Texas A&M and Missouri in our conference this year has made the diving levels a lot higher, and we don't have a 10-meter platform, so we are up there competing with the rest of the conference that has full facilities. My hats off to Cole for being able to compete. He didn't really miss anything. That was our third time on the 10-meter this year. Our last practice on it was in January. I'm pretty proud of him. I think next year we will do a little bit better."
Florida won its 34th men's SEC title with a total of 1,408, snapping Auburn's 16-year streak at the top. The Tigers finished runner-up with a score of 1,196. On the women's side, Georgia won its fourth straight title with a total of 1,420.
The Gamecock divers will be back in action on March 11-13 at the NCAA Zone B Diving Championships, which will be held in Knoxville, Tenn. The South Carolina swimmers will await word on who will be going to the NCAA Championships. The Gamecocks left College Station with two NCAA automatic qualifying times, as Flach recorded a 4:15.32 in the 500 freestyle and the men's 800 freestyle relay team turned in a 6:23.99. Both times were school records. The women's (March 21-23) and men's (March 28-30) NCAA Championships will both be held in Indianapolis, Ind.
Saturday, February 23
2013 SEC Swimming & Diving Championships
College Station, Texas – Student Recreation Center Natatorium
Day 5 Finals
Men's 100 Freestyle
16. Alex Fitton 44.41
Men's 200 Breaststroke
14. Matt Navata 1:58.53 (NCAA B cut, PR)
23. Alex Vance 2:02.67
Women's 200 Breaststroke
8. Amanda Rutqvist 2:11.66 (NCAA B cut, PR)
Men's 1650 Freestyle
16. M. El Kamash 15:19.58 (NCAA B cut, PR)
25. Alex Eiden 15:29.57 (NCAA B cut, PR)
29. Matt Columbus 15:40.92
32. Brooks Ross 15:44.95
Women's 1650 Freestyle
22. Whitney Avers 17:00.28 (PR)
24. Jordan Gibbs 17:05.07
28. Ashleigh Ferguson 17:22.15 (PR)
31. Elise Costa 17:46.70 (PR)
33. Charlotte Ward 18:18.75
Men's 400 Freestyle Relay
9. Flach, Warner, Rodriguez, Fitton 2:56.71
Women's 400 Freestyle Relay
12. Raczkowski, Drake, Bixler, Schaffer 3:25.69
Team Standings
1. Florida 1408
2. Auburn 1196
3. Georgia 1024
4. Tennessee 787.5
5. Missouri 779.5
7. Texas A&M 709.5
8. South Carolina 540.5
9. Kentucky 452.5
10. Alabama 451
1. Georgia 1420
2. Texas A&M 1296
3. Florida 1190.5
4. Tennessee 1018
5. Auburn 860
6. Arkansas 594
8. Missouri 487
9. Kentucky 368.5
10. Alabama 353
11. South Carolina 248
12. Vanderbilt 183