Inhibitory factors to human immunodeficiency virus type 1 (HIV-1) in saliva may be responsible for the infrequent isolation of virus from saliva and also may account for the marked infrequency of salivary and/or oral transmission of HIV-1. Incubation of HIV-1 with human saliva followed by addition of the mixture to susceptible cells leads to partial or complete suppression of viral replication in vitro. We investigated the inhibitory effects of whole saliva and specific glandular salivas on HIV-1 infectivity as measured by viral-induced cytopathic effects in susceptible cells. Whole saliva contained marked inhibitory activity to HIV-1, strain HTLV-IIIB, and to virus infected cells. Submandibular saliva contained inhibitory activity, but of lesser quantity. Parotid saliva demonstrated no HIV-inhibitory activity. Whole saliva also appeared to contain filterable components that were inhibitory to lymphocyte growth. Passage through a .45 micron pore-size filter eliminated the viral inhibitory activity of submandibular saliva and some of the activity in whole saliva. All salivas except parotid incubated with HIV-1 followed by filtration were inhibitory suggesting that complexing of virus with high molecular weight, submandibular mucins may play a role in viral inhibition.

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Whole saliva samples collected from available people at risk in Boston for infection with human T-lymphotropic virus type III (HTLV-III/LAV), from late 1984 through early 1985, were analyzed for the presence of antibodies to viral proteins. Fourteen of 20 (70%) acquired immunodeficiency syndrome (AIDS) patients and 14 of 15 (93%) AIDS- related complex (ARC) patients had salivary antibodies that reacted with the virus-encoded glycoproteins gp160 and gp120 of HTLV-III infected cells. All of the AIDS and ARC patients had serum antibodies to the same antigens. Of 20 sex partners of AIDS/ARC patients, nine (45%) showed anti-HTLV-III antibodies, and four of 18 (22%) healthy homosexual males also were positive for such antibodies. Serum and salivary antibody status were the same in these groups. A minority of those patients positive for salivary antibodies to env gene-encoded gp160 and gp120 also had salivary antibodies to gag gene-encoded proteins of 55,000, 24,000, and/or 17,000 daltons. Immunoglobulin A (IgA) class antibodies comprised the majority of the salivary antibody response. The spectrum of HTLV-III proteins detected by the salivary and serum antibodies was similar. The possibility that secretory IgA from the gut-associated lymphoid system may play a role to restrict salivary transmission of HTLV-III should be considered.

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