Instruct: Given a question, retrieve relevant documents that can help answer the question.
Query: Is there a cure for herpes simplex?
Since the introduction of the nucleoside analogs decades ago, treatment of herpes simplex virus (HSV) infections has not seen much innovation, except for the development of their respective prodrugs (Aciclovir, Famciclovir, Valacilovir..). Drawbacks such as poor bioavailability or limited effectiveness of these drugs require further research effort of new pharmaceutical drugs against the herpes simplex disease. The inhibitors of the Helicase-primase complex of HSV represent a very innovative approach to the treatment of herpesvirus disease.
There are no pharmaceuticals approved specifically for treating HHV-6 infection, although the usage of "Cytomegalovirus" treatments (valganciclovir, ganciclovir, cidofovir, and foscarnet) have shown some success. These drugs are given with the intent of inhibiting proper DNA polymerization by competing with deoxy triphosphate nucleotides or specifically inactivating viral DNA polymerases.
Neither a cure for SS nor a specific treatment is known to permanently restore gland secretion. Instead, treatment is generally symptomatic and supportive.
Human herpesvirus 7 (HHV-7) is one of nine known members of the Herpesviridae family that infects humans. HHV-7 is a member of Betaherpesviridae, a subfamily of the Herpesviridae that also includes HHV-6 and "cytomegalovirus" (HHV-5 or HCMV). HHV-7 often acts together with HHV-6, and the viruses together are sometimes referred to by their genus, "Roseolovirus". HHV-7 was first isolated in 1990 from CD4+ T cells taken from peripheral blood lymphocytes.
Scrapie is a fatal infectious disease of the neural system of sheep; one of a class of brain diseases that can affect cattle (BSE) and humans (Kuru, nCJD). Scrapie had been thought to be caused by a 'slow virus' – one that could take years to show as a change in behaviour or movement. By the mid 1960s, it was established that cells could only replicate via DNA. Radioactivity stops cell replication by 'killing' DNA. Alper found that radiation did not kill the infective agent in scrapie, suggesting that a virus was unlikely to be the infective agent. The infective agent had to be smaller and simpler than (viral) DNA. Alper also found that the agent remained active under ultraviolet light. DNA is inactive under UV light. Instead, the agent was killed by light at 237 nm, a wavelength specific to polysaccharide inactivation. Alper and colleagues reported these properties of the scrapie agent – a finding that was greeted with astonishment in many quarters, for it appeared to contravene the central dogma that holds that replication (and hence the growth of the disease and its infectious properties) can only proceed via DNA. However, once these empirical findings were accepted, several theories developed to accommodate the peculiar properties of the scrapie agent. The most widely accepted theory today is the prion theory, which posits a 'rogue' protein as the infectious source. However, Alper could not accept that a protein 'mutation' was the agent. Firstly, her UV radiation studies did not indicate a protein agent and, secondly, isolated prions did not induce scrapie. Her own theories concerning the agent were developed in the last years of her life and suggested a more dynamic and complex story.
Varicella is a herpes virus that causes chicken pox and shingles. Administration of the varicella vaccine during pregnancy is contraindicated. Immunity status to varicella should be elicited during the preconception counseling visit.
The HIV genome presented several additional mysteries. The virus genome contained regions that might specify as yet unknown proteins. The Haseltine laboratory discovered a novel transacting protein and a second protein, both required for virus replication. They named the transactivator tat and the second protein art; the latter was renamed rev. He predicted that drugs that target these proteins will also be effective in treating the infection. A drug that inhibits the "rev" protein has been approved by the USA Food and Drug administration for treatment of HIV infection. His laboratory went on to discover additional viral genes and proteins – "vpr", "vpu", "vif", and "nef" - required for efficient virus growth in some but not all circumstances. The discoveries were summarized in an article in 1988 in "Scientific American".
Scrapie is a fatal, degenerative disease that affects the nervous systems of sheep and goats. It is one of several transmissible spongiform encephalopathies (TSEs), which also includes bovine spongiform encephalopathy (BSE or "mad cow disease"), Creutzfeldt-Jakob disease (CJD) in humans, and chronic wasting disease in deer. Like other spongiform encephalopathies, the cause of scrapie is unknown, but is thought to be caused by an infectious misfolded protein called a prion. Scrapie has been known since 1732, and does not appear to be transmissible to humans.
Human herpesvirus 6 (HHV-6) is the common collective name for human herpesvirus 6A (HHV-6A) and human herpesvirus 6B (HHV-6B). These closely related viruses are two of the nine herpesviruses known to have humans as their primary host.
With a series of operations or even a heart transplant, a newborn can be treated but not be cured. Young individuals who have undergone reconstructive surgery must refer to a cardiologist who is experienced in congenital heart diseases, "Children with HLHS are at an increased level for developing endocarditis." Kids that have been diagnosed with HRHS must limit the physical activity they participate in to their own endurance level.
The 2008 Nobel Prize in Physiology or Medicine was awarded to Montagnier and Françoise Barré-Sinoussi for the discovery of HIV. They shared the Prize with Harald zur Hausen, who discovered that human papilloma viruses can cause cervical cancer. Montagnier said he was "surprised" that Robert Gallo was not also recognized by the Nobel Committee: "It was important to prove that HIV was the cause of AIDS, and Gallo had a very important role in that. I'm very sorry for Robert Gallo." According to Maria Masucci, a member of the Nobel Assembly, "there was no doubt as to who made the fundamental discoveries."
For decades biologists had been at work on the medicine that became penicillin. In 1928, Scottish biologist Alexander Fleming discovered a substance that killed a number of disease-causing bacteria. In 1929, he named the new substance "penicillin". His publications were largely ignored at first, but it became a significant antibiotic in the 1930s. In 1930, Cecil George Paine, a pathologist at Sheffield Royal Infirmary, used penicillin to treat sycosis barbae, eruptions in beard follicles, but was unsuccessful. Moving on to ophthalmia neonatorum, a gonococcal infection in infants, he achieved the first recorded cure with penicillin, on November 25, 1930. He then cured four additional patients (one adult and three infants) of eye infections, but failed to cure a fifth.
In 1984, Essex identified gp120, the virus surface protein that is used worldwide for blood screening, HIV detection, and epidemiological monitoring. With collaborators, he discovered the first simian immunodeficiency virus, as well as HIV-2. Since 1986, he has developed programs for AIDS collaboration in Senegal, Thailand, Botswana, India, Mexico, and China. In 1996, Essex helped establish the Botswana–Harvard Partnership for HIV Research and Education (now the Botswana–Harvard AIDS Institute). This is a collaboration between the Ministry of Health in Botswana and HAI.
Transmission is believed to occur most frequently through the shedding of viral particles into saliva. Both HHV-6B and HHV-7 are found in human saliva, the former being at a lower frequency. Studies report varying rates of prevalence of HHV-6 in saliva (between 3–90%), and have also described the salivary glands as an in vivo reservoir for HHV-6. The virus infects the salivary glands, establishes latency, and periodically reactivates to spread infection to other hosts.
The second half of the 20th century was the golden age of virus discovery and most of the over 2,000 recognised species of animal, plant, and bacterial viruses were discovered during these years. In 1957, equine arterivirus and the cause of Bovine virus diarrhoea (a pestivirus) were discovered. In 1963, the hepatitis B virus was discovered by Baruch Blumberg, and in 1965, Howard Temin described the first retrovirus. Reverse transcriptase, the enzyme that retroviruses use to make DNA copies of their RNA, was first described in 1970, independently by Howard Martin Temin and David Baltimore. In 1983 Luc Montagnier's team at the Pasteur Institute in France, first isolated the retrovirus now called HIV. In 1989 Michael Houghton's team at Chiron Corporation discovered Hepatitis C.
Another group working contemporaneously with the Montagnier and Gallo groups was that of Dr. Jay Levy at the University of California, San Francisco. He independently discovered the AIDS virus in 1983 and named it the AIDS associated retrovirus (ARV). This virus was very different from the virus reported by the Montagnier and Gallo groups. The ARV strains indicated, for the first time, the heterogeneity of HIV isolates and several of these remain classic examples of the AIDS virus found in the United States.
Treatment for cystic hygroma involves the removal of the abnormal tissue; however complete removal may be impossible without removing other normal areas. Surgical removal of the tumor is the typical treatment provided, with the understanding that additional removal procedures will most likely be required as the lymphangioma grows. Most patients need at least two procedures done for the removal process to be achieved. Recurrence is possible but unlikely for those lesions able to be removed completely via excisional surgery. Radiotherapy and chemical cauteries are not as effective with the lymphangioma than they are with the hemangioma. Draining lymphangiomas of fluid provides only temporary relief, so they are removed surgically. Cystic Hygroma can be treated with OK432 (Picibanil).
"O. tsutsugamushi" causes a complex and dangerous infection scrub typhus. Infection starts when chiggers bite on the skin during their feeding. The bacteria are deposited at the site of feeding (inoculation), where they multiply. They cause progressive tissue damage (necrosis). Necrosis progresses to inflammation of the blood vessels called vasculitis. This in turn causes inflammation of the lymph nodes, called lymphadenopathy. Within a few days, vasculitis extends to various organs including liver, brain, kidney, meninges and the lung. The disease is responsible for nearly a quarter of all the febrile (high fever) illness in endemic areas. Mortality in severe case or due to improper treatment or misdiagnosis may be as high as 30-70%. About 6% of infected people die untreated, and 1.4% of the patients die even with medical treatment. Moreover, death rate can be as high as 13% where medical treatment is not properly handled. In cases of misdiagnosis and failure of treatment, systemic complications rapidly develop including acute respiratory distress syndrome, acute kidney failure, encephalitis, gastrointestinal bleeding, hepatitis, meningitis, myocarditis, pancreatitis, pneumonia, septic shock, sub-acute thyroiditis, and multi-organ dysfunctions. Harmful symptoms involving multiple organ failure and neurological impairment are difficult to treat, and can be lifelong debilitation or directly fatal. The central nervous system is often affected and result in various complications including cerebellitis, cranial nerve palsies, meningoencephalitis, plexopathy, transverse myelitis, neuroleptic malignant syndrome, and Guillan-Barré syndrome. Death rates due to complications can be up to 14% in brain infections, and 24% with multiple organ failure. It is the major cause of acute encephalitis syndrome in India, where viral infection Japanese encephalitis has been regarded as the main factor.
The last cases of smallpox in the world occurred in an outbreak of two cases (one of which was fatal) in Birmingham, United Kingdom, in 1978. A medical photographer, Janet Parker, contracted the disease at the University of Birmingham Medical School and died on 11 September 1978. Professor Henry Bedson, the scientist responsible for smallpox research at the university, killed himself. All known stocks of smallpox were subsequently destroyed or transferred to two WHO-designated reference laboratories with BSL-4 facilities – the United States' Centers for Disease Control and Prevention and Russia's State Research Center of Virology and Biotechnology VECTOR.
"With scrapie, the archetypical TSE, which is a natural disease in sheep and goats, the disease can appear suddenly in a flock in the absence of any known exposure to infected flocks (Palsson, 1979). Finally, fields in Iceland, that were left empty for up to 3 years after the destruction of scrapie-infected flocks, were repopulated with known scrapie-free sheep, and some of the sheep in this latter group subsequently developed scrapie (Palsson, 1979). This last 'experiment in nature' has yielded similar results a number of times in Iceland and in the United Kingdom. In one Icelandic farm, flocks have been eradicated three times; each time, the farm was left without sheep for 2 years, and after restocking with sheep from scrapie-free areas, the disease reappeared. Several years ago, a suggestion was made (S Sigurdarson, personal communication) that hay mites would be a good candidate as a vector for scrapie; this led to infection of mice with mite samples prepared from hay obtained from five Icelandic farms. Ten of these 71 mice became sick after injection with mite preparations from three of the five farms (Wisniewski et al, 1996; Rubenstein et al, 1998). The incubation periods ranged from 340 days to 626 days, and these mice had the protease-resistant form Prp of a host-coded glycoprotein, PrP . The protease-resistant form is a marker of TSE disease (Prusiner, 1991; Parchi et al, 1996). For some of these clinically positive mice, the banding pattern on WB analysis was unique (Wisniewski et al, 1996; Rubenstein et al, 1998)."
The last major European outbreak of smallpox was in 1972 in Yugoslavia, after a pilgrim from Kosovo returned from the Middle East, where he had contracted the virus. The epidemic infected 175 people, causing 35 deaths. Authorities declared martial law, enforced quarantine, and undertook widespread re-vaccination of the population, enlisting the help of the WHO. In two months, the outbreak was over. Prior to this, there had been a smallpox outbreak in May–July 1963 in Stockholm, Sweden, brought from the Far East by a Swedish sailor; this had been dealt with by quarantine measures and vaccination of the local population.
The risk of transmission from mother to baby is highest if the mother becomes infected around the time of delivery (30% to 60%), since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child. In contrast, the risk falls to 3% if the infection is recurrent, and is 1–3% if the woman is seropositive for both HSV-1 and HSV-2, and is less than 1% if no lesions are visible. Women seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1-seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g. fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect caesarean section to reduce exposure of the child to infected secretions in the birth canal. The use of antiviral treatments, such as aciclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.
Herpes is contracted through direct contact with an active lesion or body fluid of an infected person. Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person. Herpes simplex virus 2 is typically contracted through direct skin-to-skin contact with an infected individual, but can also be contracted by exposure to infected saliva, semen, vaginal fluid, or the fluid from herpetic blisters. To infect a new individual, HSV travels through tiny breaks in the skin or mucous membranes in the mouth or genital areas. Even microscopic abrasions on mucous membranes are sufficient to allow viral entry.
No method eradicates herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and paracetamol (acetaminophen) can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine, or tetracaine can also relieve itching and pain.
Herpes antiviral therapy began in the early 1960s with the experimental use of medications that interfered with viral replication called deoxyribonucleic acid (DNA) inhibitors. The original use was against normally fatal or debilitating illnesses such as adult encephalitis, keratitis, in immunocompromised (transplant) patients, or disseminated herpes zoster. The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C, later marketed under the name cytosar or cytarabine. The usage expanded to include topical treatment of herpes simplex, zoster, and varicella. Some trials combined different antivirals with differing results. The introduction of 9-β-D-arabinofuranosyladenine, (ara-A or vidarabine), considerably less toxic than ara-C, in the mid-1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U.S. Food and Drug Administration in 1977. Other experimental antivirals of that period included: heparin, trifluorothymidine (TFT), Ribivarin, interferon, Virazole, and 5-methoxymethyl-2'-deoxyuridine (MMUdR). The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA aciclovir, in the late 1970s raised antiviral treatment another notch and led to vidarabine vs. aciclovir trials in the late 1980s. The lower toxicity and ease of administration over vidarabine has led to aciclovir becoming the drug of choice for herpes treatment after it was licensed by the FDA in 1998. Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, which did not occur when compared with increased dosages of vidarabine. However, aciclovir seems to inhibit antibody response, and newborns on aciclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.