According to a paper in Saturday's Lancet, oral sex can spreadAIDS via a cold sore or fever blister. Both of these terms arecolloquialisms for a viral infection on the lip caused by herpessimplex virus labialis (HSV-1. It is distinct from Herpesvirusgenitalis (HSV-2), which produces genital lesions.

Dermatologist Madalene Heng of UCLA's San Fernando ValleyInternal Medicine Program is the principal author of the Lancetarticle, which describes this previously unreported contagionpathway. The article is titled "Co-infection and synergy ofhuman immunodeficiency virus-1 and herpes simplex virus-1."

For obvious seismologically related reasons Heng was notavailable to be interviewed by BioWorld.

She and her co-authors found in vivo proof that an AIDSpatient with a cold sore can pass on the HIV-1 viral particlestranscutaneously, along with the herpes virions.

HIV's port of entry into host cells, Heng noted, uses the CD4molecule expressed by helper T cells as its receptor.Keratinocytes, the skin cells that form the surface layer on thelip, lack that CD4, so normally are proof against HIV infection.On the other hand, they are the favorite eruption site forherpesvirus-1 infection.

Some 70 percent to 90 percent of the world's population carriesantibodies to HSV-1, which lurks in the trigeminal nerveganglions near the cheek bones. Physical and perhapspsychological stresses are thought to trigger fever blisterssporadically. They occur when HSV-1 travels from its nerve-cell hideaway to the lip and replicates.

Heng took 4-millimeter punch biopsies from the skin of sixmale AIDS patients, 25 to 47 years of age, who were free ofherpes lesions. Another six age- and sex-matched men withfrequent fever blisters but without AIDS supplied controlbiopsies. She examined these specimens by both light andelectron microscopy. Skin-cell specimens were also incubatedwith polyclonal antibodies to HSV-1, and monoclonals to HIV'sp24 core antigen.

Electron microscopy revealed co-infection of keratinocytes andmacrophages by multiple virions of both HSV-1 and HIV-1. Theaverage number of such particles per infected keratinocyte was736.3 -- far higher than the 31.2 in non-AIDS herpes patientsand zero in herpes-free AIDS subjects

Recalling in her paper that "concomitant infections by HIV-1and cytomegalovirus, a herpesvirus, results in infection of non-CD4-bearing brain tissue," Heng speculated that "the associationof HIV-1 envelope proteins with HSV-1 proteins ... may allowHIV-1 to retain its infectivity without the need for the CD4molecule for cell entry."

Other visual evidence from microscopy, the bulkier andmisshapen appearance of virions in infected cells, suggestedthat both species of virus may have actually hybridized in vivo.And many of the infected cells seemed to release both kinds ofinfective particles into the extracellular fluid. This may haveepidemiological significance in the transcutaneous transmissionof the virus.

Other than "saying no" to oral sex, what can be done to sidestepthis risk factor? Heng urges inclusion of anti-herpetic drugs inoverall AIDS therapy. This, she argued, would "avoid excessivereplication of HIV-1 in CD4-dependent and independenttargets." She bolstered this proposal by citing recentlypublished clinical data showing increased survival of AIDSpatients treated with acyclovir as well as AZT.

-- David N. Leff Science Editor

(c) 1997 American Health Consultants. All rights reserved.