No abstract

Human cytomegalovirus (HCMV) is a potential cofactor in HIV-1 infection. To investigate the mechanism whereby HCMV promotes HIV-1 replication, a PBMC coculture assay which measures HIV-1 p24 antigen release was used as an index ofviral replication. HCMV-stimulated PBMC were capable of inducing HIV-1 replication in cocultures with acutely infected PBMC; however, this occurred only when the PBMC were from HCMV-seropositive donors (598±207 versus 27±10 pg/ml p24 antigen with PBMC from HCMV-seronegative donors on day 6 of coculture). Upon stimulation with HCMV, PBMC obtained exclusively from HCMV-seropositive donors released tumor necrosis factor (TNF)-a (270±79 pg/ml at 18 h of culture). Monoclonal antibodies to TNF-a blocked the activity of HCMV-stimulated PBMC in cocultures both with acutely HIV-1-infected PBMC and with the chronically infected promonocytic line U1. Also, treatment of HCMV-stimulated PBMC with pentoxifylline, an inhibitor of TNF-a mRNA, markedly reduced HIV-1 replication in cocultures both with acutely and chronically infected cells. These results indicate that TNF-a is a key mediator of HIV-1 replication induced by HCMV-stimulated PBMC and support the concept that this cytokine plays an important role in the pathogenesis of HIV-1 infection. (J. Clin. Invest. 1992. 89:574-580.)

No abstract

An immunocompromised woman died of disseminated infection due to adenovirus type 3. During her hospitalization and after her death, 38 hospital personnel developed an acute respiratory illness. Adenovirus type 3 infection was documented by culture in 18 of the 38 individuals and by seroconversion in one additional employee. Four of 34 asymptomatic hospital personnel exposed to the index case also seroconverted. Thus, 23 personnel were considered to have confirmed infections, and 22 of these 23 reported direct contact with the index case. Acquisition of infection was associated with the number and type of contacts. Protection against infection was associated with detectable serum-neutralizing antibody in the early serological sample. Restriction enzyme analysis using six different endonucleases indicated that all isolates of virus were type 3a and had identical genetic composition. This study underscores the importance of adenovirus as a cause of nosocomial infection and indicates that genetic analysis of viral DNA is a powerful tool for studying common-source outbreaks.

Immunocompetent children, adolescents and adults with chickenpox displayed a gradation in their clinical responses to acyclovir that correlated with the time from onset of rash to initiation of therapy. Five days of therapy is sufficient because a 7-day course provided no additional benefit. The susceptibility to acyclovir of viruses shed during treatment did not change; however, the effect of therapy on resistance of latent virus was not assessed.