HIV infects immune cells, mainly CD4+ T cells. But they are not the only ones. It also settles in the genome of myeloid cells, monocytes or macrophages. According to a study from Johns Hopkins University, the viral DNA inserted into myeloid cells is functional. The virus also reactivated from the monocyte-derived macrophage reservoir. New cure strategies need to take these cells into account to eradicate the virus from the body.
The mechanisms behind the mortality associated with early antiretroviral therapy (ART) treatment in children infected perinatally with HIV are poorly understood. Researchers sought to find potential biomarkers associated with the increased mortality. They created three groups of subjects: deceased (dead HIV+, n=20), nondeceased HIV+ (HIV+, n=59) and healthy controls (n=13).
Researchers from IrsiCaixa Institute for AIDS Research presented data from a study that aimed to identify biomarkers associated with virus control during monitored antiretroviral pause (MAP) in patients with HIV.
A lot of focus has been put on targeting T-cell immunoreceptor with Ig and ITIM domains (TIGIT) for HIV infection treatment, but no attention has been given to targeting its ligand, CD155.
Antiretroviral (ARV) therapy suppresses HIV, but viral replication rebounds once treatment is discontinued. The redistribution of lipids in the plasma membrane to form microdomains is crucial for viral entry and biogenesis during HIV infection. Researchers at Johns Hopkins University School of Medicine found neutral sphingomyelinase 2 (nSMase2) to be a key component of the late stages of HIV viral assembly and maturation; they hypothesized that nSMase2 inhibitors could help avoid viral rebound.
To date, there is a lack of consensus in anal cancer screening. DNA methylation markers zing finger protein 582 (ZNF582) and achaete-scute homolog 1 (ASCL1) have been associated with anal intraepithelial neoplasia (AIN3) and anal carcinoma risk in people with HIV infection.
The intestinal microbiota could protect against HIV infection. At the 30th Conference on Retroviruses and Opportunistic Infections (CROI) last week, a group of scientists from Duke University presented data showing a preventive effect of two bacteria from the Lachnospiraceae family, the species Clostridium immunis and Ruminococcus gnavus against HIV. These microorganisms strongly inhibited HIV replication in vitro through the metabolic pathway of tryptophan and the aryl hydrocarbon receptor.
HIV research is a winding road where one obstacle leads to another, slowing down success. The first barrier to getting the cure starts before one can even talk about it. “Cure may be too powerful and promising a term. Remission is probably better,” said John Mellors, whose work led to the universal use of plasma HIV-1 RNA and CD4+ T-cell counts in HIV-1 infection.
“Cure means maintaining an undetectable viral load off antiretroviral treatment. That means you cannot transmit it to people. Within that definition, there are people that have complete eradication of every single virus. And then, you have people that have a low level of virus that are able to keep under control without drugs,” Sharon Lewin told BioWorld. “Remission is maintaining a viral load less than 50 copies per milliliter in the absence of any retroviral. But there is still virus detectable,” she explained. Lewin is the director of The Peter Doherty Institute for Infection and Immunity in Melbourne, and the president of the International AIDS Society (IAS).
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