HIV - Type 1 Productive Infection with X 4 and R 5 T Cells More Susceptible to + Memory CD 4 TLR 2 Signaling Renders Quiescent

TLR 2 Signaling Renders Quiescent Naive and Memory CD 4 T Cells More Susceptible to Productive Infection with X 4 and R 5 HIV - Type 11

It has been recently demonstrated that circulating microbial products are responsible for a systemic immune activation in individuals infected with HIV-type 1. Bacterial products carry structural conserved motifs recognized by TLRs. Some TLR members are expressed in primary human CD4 T cells but the precise functional role played by these pattern recognition receptors is still imprecise. In thi...

Tat protein induces self-perpetuating permissivity for productive HIV-1 infection.

We report that human immunodeficiency virus type 1 (HIV-1) has evolved a self-perpetuating mechanism to actively generate cells permissive for productive and cytopathic infection. Only activated T cells can be productively infected, which leads to their rapid depletion (2 x 10(9)/day in an infected individual). Establishment of productive HIV-1 infection therefore requires continual activations...

Expression of Integrin Type 1 Infection Regardless of Their Preferential Targets for Productive HIV T Cells Are + CD 4 + Memory CCR

LFA-1 is a key determinant for preferential infection of memory CD4+ T cells by human immunodeficiency virus type 1.

Memory CD4+ T cells are considered a stable latent reservoir for human immunodeficiency virus type 1 (HIV-1) and a barrier to eradication of this retroviral infection in patients under therapy. It has been shown that memory CD4+ T cells are preferentially infected with HIV-1, but the exact mechanism(s) responsible for this higher susceptibility remains obscure. Previous findings indicate that i...

Virion encapsidated HIV-1 Vpr induces NFAT to prime non-activated T cells for productive infection

The majority of T cells encountered by HIV-1 are non-activated and do not readily allow productive infection. HIV-1 Vpr is highly abundant in progeny virions, and induces signalling and HIV-1 LTR transcription. We hence hypothesized that Vpr might be a determinant of non-activated T-cell infection. Virion-delivered Vpr activated nuclear factor of activated T cells (NFAT) through Ca(2+) influx a...