Fox Chase Chemical Diversity Center Inc. and University of Pittsburgh have jointly described new proteolysis targeting chimeras (PROTACs) consisting of Nef (HIV-1)-targeting moiety covalently linked to cereblon (CRBN)-binding moiety.
After a five-year court battle in which Gilead Sciences Inc. scored several victories only to have the U.S. government appeal, Gilead has reached a settlement with the Department of Health and Human Services and the Department of Justice to resolve government claims that the company had infringed its patents covering the pre-exposure prophylaxis (PrEP) use of two Gilead HIV drugs.
First, the good news about pandemics – and in 2024, there was big “good news.” Science Magazine named lenacapavir (Gilead Sciences Inc.) as the Breakthrough of the Year. In two separate trials, lenacapavir prevented HIV transmission with 100% efficacy in cisgender African women and 99.9% efficacy in men and gender-diverse persons when administered twice a year.
Antiretroviral therapy effectively suppresses HIV viral loads to undetectable levels but cannot eliminate the integration of viral DNA into the host cell genome.
In a recent publication, researchers from Colorado State University presented the development and evaluation of humanized mice as a hybrid dual-use model for testing therapeutics against both HIV and SIV infections.
Gilead Sciences Inc. recently disclosed details on the work that led to the discovery of elunonavir (GS-1156), an unboosted HIV protease inhibitor currently in phase I studies.
HIV-1 infects lymphocytes and macrophages, gradually destroying the immune system. Multiple treatment combinations suppress the viral load to undetectable levels, but their long-term use leads to adverse effects. Allosteric inhibition of HIV-1 integrase has emerged as a source for new treatment strategies.
In mammals, the disruptor of telomeric silencing 1-like (DOT1L) is the only methyltransferase that catalyzes the mono-, di- and tri-methylation of histone H3 at lysine 79 (H3K79). The DOT1L/H3K79me is involved in several relevant physiological and pathological mechanisms, including several viral infections.
A strategy inspired by deficient HIV replication could be used as a treatment to reduce viral load in patients living with HIV and help control the pandemic of the retrovirus. Scientists from the University of California San Francisco want to use HIV against itself by using a parasitic version of the pathogen.
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