Jun.28,2007  3  US 2007/0148124 Al  therapeutic regimens is the emergence of HIV mutants that  are resistant to single or even multiple medications. Such  drug-resistance HIV works against the population in two  ways. First, the infected individual will eventually run out of  treatment options; and second, if the infected individual  passes along a virus already resistant to many existing  therapeutic agents, the newly infected individual will have a  more limited treatment option.  [0024]  The HIV-1 replication cycle can be interrupted at  many different points. As indicated by the approved medi› cations, viral reverse transcriptase and protease enzymes are  good molecular targets, as is the entire process by which the  virus fuses to and injects itself into host cells. Thus the  recently approved drug T20 (Fuzeon) is the first in a novel  class ofanti-HIV-1 agents. However, in addition to the drugs  already approved for treatment of HIV-1 infection, work  continues on the discovery and development of additional  treatment modalities. This is necessary because of the pro› pensity of the virus to mutate and thus render ineffective the  existing therapies.  [0025]  The search for chemotherapeutic interventions that  work by novel mechanism( s) of action is particularly impor› tant in the search for new medications to combat the spread  of the HIV. Several potential areas for intervention that are  under consideration or have active programs include 1)  blocking the viral envelope glycoprotein gp120, 2) addi› tional mechanisms beyond gp120 to block virus entry, such  as blocking the virus receptor CD4 or co-receptors CXCR4  or CCR5, 3) viral assembly and disassembly through tar› geting the zinc finder domain of the viral nucleocapsid  protein 7 (NCp7) and 4) interfering with the functions of the  viral integrase protein and interrupting virus specific tran› scription processes.  [0026]  The mechanism by which HIV passes through the  mucosa! epithelium to infect underlying target cells, in the  form of free virus or virus-infected cells, has not been fully  defined. In addition, the type of cells infected by the virus  could be derived from any one, or more, of a multitude of  cell types (Miller, C. J. et al. "Genital Mucosa! Transmission  of Simian Immunodeficiency Virus: Animal Model for Het› erosexual  Transmission of Human Immunodeficiency  Virus."J.  Viral.  63:4277-4284 (1989); Phillips, D. M. and  Bourinbaiar, A. S. "Mechanism of HIV Spread from Lym› phocytes to Epithelia."Virology 186, 261-273 (1992); Phil› ips, D. M., Tan X., Pearce-Pratt, R. and Zacharopoulos, V.  R., "An Assay for HIV Infection of Cultured Human Cervix› derived Cells."J.  Viral. Methods,  52, 1-13 (1995); Ho, J. L.  et al, "Neutrophils from Human Immunodeficiency virus  (HIV)-seronegative Donors Induce HIV Replication from  HIV-infected patients Mononuclear Cells and Cell lines. An  In Vitro Model of HIV Transmission Facilitated by  Chlamy› dia Trachomatis."  J. Exp. Med.,  181, 1493-1505 (1995);  Braathen, L. R., and Mork, C., in "HIV infection of Skin  Langerhans Cells", In: Skin Langerhans (dendritic) cells in  virus infections and AIDS (ed Becker, Y.) 131-139, Kluwer  Academic Publishers, Boston, (1991)). Such cells include T  lymphocytes, monocytes/macrophages and dendritic cells,  suggesting that CD4 cell receptors are engaged in the  process of virus transmission as is well documented for HIV  infection in blood or lymphatic tissues (Parr M. B., and Parr  E. L., "Langerhans Cells and T lymphocytes Subsets in the  Murine Vagina and  Cervix."Biology and Reproduction  44,491-498 (1991); Pope, M. et al. "Conjugates ofDendritic  Cells and Memory T Lymphocytes from Skin Facilitate  Productive Infection With HIV-1."Cell 78, 389-398 (1994);  and Wira, C. R. and Rossoll, R. M. "Antigen-presenting  Cells in the Female Reproductive Tract: Influence of Sex  Hormones on Antigen Presentation in the  Vagina."Immunol› ogy,  84, 505-508 (1995)).  [0027]  Therefore, the need for efficacious, safe, and inex› pensive anti-viral agents to treat or prevent the transmission  of HIV (in lieu of a vaccine) is evident.  [0028]  Besides HIV, herpes viruses also infect humans  ("Herpesviridae; A Brief Introduction",  Virology,  Second  Edition, edited by B. N. Fields, Chapter 64, 1787 (1990))  and cause STDs. Some common herpes viruses are  described below. However, the list is not meant to be  exhaustive, but only illustrative of the problem.  [0029]  Herpes Simplex Virus Type 1 (HSVl) is a recurrent  viral infection characterized by the appearance on the cuta› neous or mucosa! surface membranes of single or multiple  clusters of small vesicles filled with clear fluid on a slightly  raised inflamed base (herpes labialis). In addition, gingivos› tomatitis may occur as a result of HSVl infection in infants  (Kleymann, G., "New antiviral drugs that target herpes virus  helicase primase enzyme." Herpes 10:46-52 (2003); "Her› pesviridae; A Brief Introduction",  Virology,  Second Edition,  edited by B. N. Fields, Chapter 64, 1787 (1990)).  [0030]  Herpes Simplex Virus Type 2 (HSV2) causes geni› tal herpes, and vulvovaginitis may occur as a result ofHSV2  infection in infants (Kleymann, G., "New antiviral drugs  that target herpes virus helicase primase enzyme." Herpes  10:46-52 (2003)).  [0031]  Human Cytomegalovirus (HCMV) infections are a  common cause of morbidity and mortality in solid organ and  haematopoietic stem cell transplant recipients (Razonable,  R. R., and Paya, C. V., "Herpes virus infections in transplant  recipients: current challenges in the clinical management of  cytomegalovirus and Epstein-Barr virus infections." Herpes  10:60-65 (2003)).  [0032]  Varicella-Zoster Virus (VZV) causes varicella  ( chickenpox) and Zoster (shingles) (Vazquez, M., "Varicella  Zoster virus infections in children after introduction of live  attenuated varicella vaccine."Curr.  Opin. Pediatr.  16:80-84  (2004)).  [0033]  Epstein-Barr virus (EBY) is the causative agent of  infectious mononucleosis and has been associated with  Burkett’s lymphoma  and  nasopharyngeal  carcinoma.  Human Herpes virus 6 (HHV6) is a very common childhood  disease causing exanthem subitum (roseola) (Boutolleau, D.,  et al., "Human herpes virus (HHV)-6 and HHV-7; two  closely related viruses with different infection profiles in  stem cell transplant recipients",  J.  Inf Dis.  (2003)).  [0034]  Herpes Simplex Virus Type 7 (HSV7) is a T-lym› photropic herpes virus and can cause exanthem subitum. The  pathogenesis and sequelae of HH7, however, are poorly  understood (Dewhurst, S., Skrincosky, D., and van Loon, N.  "Human Herpes virus  7", Expert Rev Mo!. Med. 18:1-10  (1997)).  [0035]  Herpes Simplex Virus Type 8 (HSV8) is another  herpes virus. The molecular genetics of the human herpes  virus 8 (HHV8) has now been characterized, and the virus  appears to be important in the pathogenesis of Kaposi’s 