An early start to long-term antiretroviral therapy limits the size of the HIV-1 reservoir more effectively than treatment that starts later.

An in-depth view of the in vivo blood and tissue HIV reservoir is presented highlighting shared phenotypic features between individuals, thus enabling marked ex vivo enrichment of replication-competent latent cells.

Bacterial gut pathogens that invade into host tissues during infection can boost the spread and accumulation of plasmids over time by forming reservoirs containing these plasmids within host tissues.

Building on previous work (Zanini et al, 2015), deep-sequencing is used to show that HIV persistence during suppressive antiretroviral therapy, the main hurdle for HIV cure, is due to homeostatic proliferation and longevity of infected cells rather than ongoing virus replication.

An analysis of innate immunity reveals why dengue viruses do not reach high titers in primate laboratory models, even though they emerged through zoonotic transmission from primate reservoirs.

Identifying and treating those groups of individuals that are most likely to transmit the malaria parasite to mosquitoes could help to control the spread of the disease.

HIV-specific T cells remain detectable for years in HIV-infected individuals on antiretroviral therapy and importantly, mostly (68%) recognize HIV viruses that have the capacity to rebound following treatment interruption.

The expression of CD32 in HIV-reservoir cells prevents the binding of specific anti-HIV antibodies conferring resistance to NK cell-mediated death, and gives the cell the potential to proliferate in the presence of immune complexes.

Mathematical models of the build-up and depletion of the hypnozoite reservoir in the liver can inform the design of treatment strategies for preventing Plasmodium vivax relapse infections.

The higher amount of cortical immature neurons in brains with expanded neocortices may represent a reservoir of young cells for mammals with reduced neurogenesis.