Therefore, this active replication of HIV-1 was occurring in otherwise asymptomatic individuals. Most of the organs we examined were from asymptomatic individuals, and all had cells that were strongly positive for intracellular viral protein. However, skin differs from adenoid mucosa in that T cells are rare within the epithelium, and most of the DCs are immature in phenotype and function. That is, the DCs lack high concentrations of major histocompatibility complex class II and accessory molecules, marked T cell stimulatory function, and the p55 actin-bundling protein. By extension, we propose that the adenoid mucosa promotes the interaction of T cells with DCs that are activated repeatedly by persistent environmental stimuli in the nasopharynx.
Viral replication occurs predominantly in syncytia in infected nasopharyngeal tissue.
We do not have access to the virus from this group of patients, all of whom are residents of the United States without a significant travel history, so we are unable to determine if the viruses with which they are infected would be classified as syncytium inducing or non-syncytium inducing with standard cell lines. However, syncytia were a standard feature of infection within the mucosa of the adenoid even in asymptomatic disease. The T cell marker may be down-regulated after fusion with DCs, or the DCs may simply require contact with T cells to support viral replication. Efforts can now be directed to determine whether DCs within the many lymphoid organs of the pharynx, collectively termed Waldeyer's ring, consistently represent a major site for HIV-1 replication early in disease. Infants who swallow virus from mothers during birth or breast feeding also may be infected initially in these tissues.