Background: Coinfection with human immunodeficiency virus (HIV) has been shown to influence the natural history of hepatitis C infection. Objective: Our interest was to determine if HIV coinfection influences the prevalence of cryoglobulinemia in hepatitis C virus (HCV) infected persons. Study design: A total of 384 HCV RNA positive (234 HIV-infected and 150 HIV-uninfected) participants were tested at two visits, 18 months apart, for HCV and HIV RNA, CD4, and liver enzyme levels. Serum cryoglobulin levels were measured at a subsequent visit for a subset of the sample. Results: HIV-infected participants had significantly higher HCV RNA levels (P < 0.0001) and aspartate transaminase (AST) levels (P < 0.0001), but not alanine transaminase (ALT) levels (P > 0.05) as compared with HIV-uninfected participants. These findings were consistent at both visits and no significant changes were observed between visits. Fifty (19%) of the 264 participants tested had detectable cryoglobulins. No difference was observed in HIV seropositivity among participants with or without cryoglobulinemia (68% versus 61%; odds ratio = 1.34, P = 0.37). However, among HIV coinfected participants, elevated AST levels (P = 0.04) and lower CD4 levels (P = 0.02) were associated with cryoglobulinemia. Conclusions: While previously reported associations were found between HIV and coinfection with HCV in this study, we did not find an association between HIV infection and cryoglobulinemia.

A potential public health concern is the reported detection of the human T-lymphotropic virus (HTLV) tax gene in the lymphocytes of up to 11% of a low-risk group of New York City blood donors (NYBD). This study aimed to independently confirm the prevalence of HTLV tax sequences in 293 NYBD. All NYBD tested negative for antibodies to HTLV types 1 and 2 and HTLV Tax. HTLV tax sequences were not detected in the NYBD lymphocytes. These data demonstrate the lack of HTLV-1 tax in this group of NYBD at low risk for HTLV infection.

Our objectives were to determine if primary epithelial cells can be infected by HIV-1 and transmit the virus to peripheral blood mononuclear cells (PBMCs). Primary prostate and cervical epithelial cells as well as epithelial cell lines were exposed to various concentrations of HIV-1 and either rinsed extensively or trypsinized and replated. Resting or activated, CD8-depleted PBMCs at several concentrations were added to selected cultures. Cell surface and mRNA expression for HIV-1 receptors and coreceptors was determined by flow cytometry and RT-PCR. Viral replication was monitored using a p24gag ELISA, and infection was determined by PCR amplification for integrated provirus. Cell-free and cell-associated HIV-1 did not infect primary epithelial cells or cell lines as determined by the lack of detectable p24 and integrated provirus. Cell surface expression was detected for galactocyl ceramide but not for R5, X4, or CD4. Interestingly, mRNA expression of X4 was observed. In cases where HIV-1 was pretreated with soluble CD4 or proteases to allow for CD4-independent viral entry into the epithelial cells, viral expression or integrated provirus was again not detected. HIV-1 was not recovered from the rinsed or replated primary epithelial cells or cell lines with resting PBMCs; however, in activated PBMCs HIV-1 was recovered from rinsed but not from replated epithelial cells. These data imply that HIV-1 transmission may occur through virus transfer or by a breakdown of the epithelial membrane integrity rather than infection of the epithelial cell directly.

Primary prostate and cervical epithelial cells and epithelial cell lines were examined for human immunodeficiency virus type 1 (HIV-1) infection or transmission to peripheral blood mononuclear cells (PBMC). Neither cell-free nor cell-associated HIV-1 infected primary epithelial cells or cell lines. Pretreatment of HIV-1 to enhance CD4-independent entry did not augment infection. Cell surface expression was detected for galactosyl ceramide but not for CC-chemokine receptor 5, CXC-chemokine receptor 4, or CD4. The ability to transfer HIV-1 to resting or activated PBMC was tested by culturing with rinsed or trypsinized and replated HIV-1-exposed epithelial cells. Virus was not recovered from the rinsed or replated cocultures with resting PBMC; however, activated PBMC recovered HIV-1 from rinsed epithelial cells and rarely from replated epithelial cells. Although urogenital epithelial cells are not infected, these data suggest that they can transfer virus to activated immune cells and have implications for sexual transmission of HIV-1.