Humanized mouse models of HIV-1 latency.
The existence of long-lasting cellular reservoirs of HIV-1 is one of the major hurdles in developing effective anti-retroviral therapies. These latently infected cells and tissues efficiently evade immune responses and remain dormant until activated, upon which they can generate a productive HIV-1 infection. This classic scenario of viral latency becomes even more difficult to study and model due to the extreme complexity of translating in vivo virus-cell interactions into a controlled in vitro system. The recent developments and constant improvements upon hematopoietic engraftment of human cells and tissues onto recipient immunocompromised murine scaffolds have made it possible to model complex human innate and adaptive immune responses in a small animal model. Specifically, HIV-1 infection has been successfully modeled in these humanized mice to mimic transmission, pathogenesis, host immune responses, and treatment. Here, we review the complexities surrounding modeling HIV-1 latency in vitro and in vivo and highlight the most recent humanized mouse models that support retroviral infection.
George Mason University, National Center for Biodefense & Infectious Diseases, School of Systems Biology, Manassas, VA 20110, USA.
Rachel V
RV
Duyne
Aarthi
A
Narayanan
Kylene
K
K-Hall
Mohammed
M
Saifuddin
Leonard
L
Shultz
Fatah
F
Kashanchi
D000818:Animals; D023241:Antiretroviral Therapy, Highly Active; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000821:virology; D004195:Disease Models, Animal; D015658:HIV Infections / Q000188:drug therapy / Q000821:virology*; D015497:HIV-1 / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D051379:Mice; D014775:Virus Activation / Q000502:physiology; D017735:Virus Latency / Q000502:physiology*