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.

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

Genome-intact HIV-1 proviruses were detected in autopsy samples from the brain of ART-treated persons living with HIV, indicating that the virus can persist in the central nervous system.

The frequency of SIV reactivation from latency after treatment interruption is not directly related to measures of SIV DNA, RNA, immune activation or immune response in peripheral blood.

Data exploring host and parasite signatures in the peripheral blood indicate that total parasite biomass is a better predictor of P. vivax-induced host responses and pathogenesis than peripheral parasitemia.

Extremely early antiretroviral therapy during HIV-1 subtype C infection leads to faster decline in genome-intact viruses, reduced genetic complexity, and immune escape, and may enhance reservoir clearance with additional interventional strategies.

Inflamasomme inhibition prevents immune activation, HIV-1 pathogenesis and the splenic content of HIV-1 total DNA in humanized mice when administrated early after HIV-1 infection.

African trypanosomes residing within the skin of infected humans represent an important yet overlooked transmissible parasite population that may thwart efforts to eliminate African sleeping sickness.

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 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.