The U.S. government’s attempts to enforce its ownership of biopharma intellectual property got a setback May 9 when a six-member federal jury in Delaware determined that Gilead Sciences Inc. did not infringe government patents claiming pre-exposure prophylaxis (PrEP) use of Gilead’s HIV drugs, Truvada and Descovy, both of which combine emtricitabine and tenofovir.
Merck Sharp & Dohme Corp. researchers have patented targeted activator of cell kill (TACK) compounds acting as Gag polyprotein (HIV-1)/protein Pol dimerization inducers and thus reported to be useful for the treatment of HIV infection.
The success of the President’s Emergency Plan for AIDS Relief (PEPFAR) over the past 20 years is one of the biggest challenges in reaching its goal of eliminating HIV as a global public health threat by 2030, members of the U.S. Senate Foreign Relations Committee were told as they moved toward reauthorizing the program for another five years.
Although COVID-19 may be more severe in people with HIV (PWH), the underlying biological mechanisms among PWH treated with antiretroviral therapy (ART) remain largely unknown.
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.
