The T4 gene encodes the AIDS virus receptor and is expressed in the immune system and the brain

HIV-1 gp120 receptor on CD4-negative brain cells activates a tyrosine kinase

“…Manifestations of ADC are progressive cognitive, motor, and behavioral dysfunctions that have been linked to the persistence of HIV-1 infections in the CNS and are mainly found in CD4-positive (CD4+) microglial cells and circulating macrophages (Budka, 1991;Fauci, 1988;Jordan et al, 1991;Ketzler et al, 1990;Liu et al, 1990;Maddon et al, 1986;McArthur, 1987;Merrill and Chen, 1991;Price et al, 1988). However, in the absence of CD4 molecules on the cell membrane of the majority of brain cells and in the light of the paucity of direct evidence for HIV infection of neurons and glial cells it has been suggested that the HIV-associated degenerative neurological abnormalities are the result of indirect mechanisms mediated by soluble factors of viral or cellular origin (Brenneman et a/., 1988;Dreyer et al, 1990;Giulian et al, 1990;Kaiser et al, 1990;Pulliam et al, 1991;Wahl et al, 1991 ).…”

Expression of the CD6 T lymphocyte differentiation antigen in normal human brain☆

“…At present the significance of the cross-reactivity between nervous elements and lymphocytes has not been clarified, but there is increasing evidence that shared antigens may be involved in the pathogenesis of immune-mediated neurologic diseases. For instance, the CD4-antigen found on hematopoietic and neural cells has been shown to bind the acquired immunodeficiency syndrome (AIDS) virus, causing both immunological and brain defects (Maddon et al, 1986;Funke et al, 1987). Furthermore, common antigens may be involved in system overlapping interactions.…”

MuLV-based vectors pseudotyped with truncated HIV glycoproteins mediate specific gene transfer in CD4+ peripheral blood lymphocytes

“…Retroviruses use a variety of receptors to enter cells; some of these receptors such as the ecotropic and amphotropic murine leukemia virus (MuLV) receptors and many of the immunodeficiency-causing lentivirus receptors have been identified. [3][4][5][6][7][8] However, targeted delivery of a murine-based retroviral vector to a specific subpopulation of human cells has yet to be truly achieved. Initial attempts to change viral tropism were done through the use of pseudotyped viruses; [9][10][11] MuLV is able to incorporate vesicular stomatitis virus G glycoprotein (VSV-G), influenza virus hemagglutinin (HA), or heterologous retroviral glycoproteins, although this expands viral host range rather than restrict cell tropism.…”