HIV induces expression of complement component C3 in astrocytes by NF-κB-dependent activation of interleukin-6 synthesis.

Background: Abnormal activation of the complement system contributes to some central nervous system diseases but the role of complement in HIV-associated neurocognitive disorder (HAND) is unclear.

Methods: We used real-time PCR and immunohistochemistry to detect complement expression in postmortem brain tissue from HAND patients and controls. To further investigate the basis for viral induction of gene expression in the brain, we studied the effect of HIV on C3 expression by astrocytes, innate immune effector cells, and targets of HIV.

Productive infection of primary murine astrocytes, lymphocytes, and macrophages by human immunodeficiency virus type 1 in culture.

A mouse model of human immunodeficiency virus type 1 (HIV-1) infection would be extremely valuable for evaluation of therapies and vaccines; however, multiple blocks to productive infection of NIH 3T3 and other mouse cell lines have been reported. The authors investigated the replication of HIV-1 in primary mouse astrocytes, lymphocytes, and macrophages in culture by infection with intact HIV-1 pseudotyped with the vesicular stomatitis virus G envelope glycoprotein (VSV-G) or with the envelope glycoprotein of amphotropic murine leukemia virus. Astrocytes, lymphocytes, and macrophages were susceptible to productive infection as variously assayed by detection of p24 and Tat proteins, viral protease-mediated processing of Gag, appropriately spliced viral RNA, and infectious progeny virus.

[Chronic hepatitis C infection--mechanisms of virus "immune escape"].

The characteristic feature of HCV infection is the presence of both humoral and cellular immune response. In spite of the immune activation the host is unable to eradicate the virus. Spontaneous resolution of chronic infection is exceedingly rare--it is estimated at 0.

[Molecular epidemiology of chronic hepatitis C (HCV) virus].

Hepatitis C virus (HCV) is a major etiologic causative agent of chronic hepatitis, cirrhosis with its attendant risks of hepatocellular carcinoma. Efforts to isolate the virus by standard immunologic and virologic techniques were unsuccessful and HCV was finally identified by direct cloning and sequencing of its genome. Although the virus was identified 15 years ago, its pathogenesis and replication are not fully understood.

A mouse model for study of systemic HIV-1 infection, antiviral immune responses, and neuroinvasiveness.

We created a model of HIV-1 infection of conventional mice for investigation of viral replication, control, and pathogenesis. To target HIV-1 to mice, the coding region of gp120 in HIV-1/NL4-3 was replaced with that of gp80 from ecotropic murine leukemia virus, a retrovirus that infects only rodents. The resulting chimeric virus construct, EcoHIV, productively infected murine lymphocytes, but not human lymphocytes, in culture.