Basic Science Award

HIV-1 latency is a state of reversible, non-productive infection that occurs primarily in long-lived memory CD4+ T cells. Latency allows infected cells to evade both the host immune response and antiretroviral drugs, thereby making it one of the most significant barriers to viral eradication. HIV-1 latency is a product of proviral transcriptional silencing and can occur both directly upon infection (primary latency), as well as by progressive silencing of productive infections (secondary latency).

HIV-1 latency is a state of reversible, non-productive infection that occurs primarily in long-lived memory CD4+ T cells. Latency allows infected cells to evade both the host immune response and antiretroviral drugs, thereby making it one of the most significant barriers to viral eradication. HIV-1 latency is a product of proviral transcriptional silencing and can occur both directly upon infection (primary latency), as well as by progressive silencing of productive infections (secondary latency).

Publications:

• PubMed# 18692772
• PubMed# 19416841

Mucosal epithelia are the first tissue sites of contact of HIV with the human body during the course of infection, and these play a critical role in determining its success in establishing systemic infection. We have shown that experimental disruption of tight junctions of mucosal epithelium may facilitate HIV transmission across mucosal epithelia by paracellular penetration, which requires no viral replication and, therefore, antiretroviral therapy would not be expected to block such transmission.

Mucosal epithelia are the first tissue sites of contact of HIV with the human body during the course of infection, and these play a critical role in determining its success in establishing systemic infection. We have shown that experimental disruption of tight junctions of mucosal epithelium may facilitate HIV transmission across mucosal epithelia by paracellular penetration, which requires no viral replication and, therefore, antiretroviral therapy would not be expected to block such transmission.

Publications:

• PubMed# 19136668
• PubMed# 18692772
• PubMed# 18692180

Publications:

• PubMed# 19136668
• PubMed# 18692772
• PubMed# 18692180

Natural killer (NK) cells have traditionally been considered members of the innate immune system. Recently, in a mouse model of cytomegalovirus, our lab has demonstrated that NK cells undergo clonal expansion during acute viral infection, the population contracts when virus is controlled, but remarkably infection induces a population of "memory" NK cells. These cells are long-lived, respond more robustly when re-challenged, and provide enhanced host protection against re-infection.

Natural killer (NK) cells have traditionally been considered members of the innate immune system. Recently, in a mouse model of cytomegalovirus, our lab has demonstrated that NK cells undergo clonal expansion during acute viral infection, the population contracts when virus is controlled, but remarkably infection induces a population of "memory" NK cells. These cells are long-lived, respond more robustly when re-challenged, and provide enhanced host protection against re-infection.