Anthony Fauci has retired from his position as director of the National Institute of Allergy and Infectious Diseases (NIAID) and as chief medical advisor to the U.S. president. But Fauci, who has advised every president since Ronald Reagan, continues to share his encyclopedic knowledge with the HIV research community, as he has since the beginning of the HIV pandemic. Fauci co-founded the first National Conference on Human Retroviruses and related infections in 1993. At the Opening Session of the 30th edition of the Conference on Retroviruses and Opportunistic Infections (CROI), he highlighted the advances that have collectively extended the life expectancy of newly diagnosed patients by decades.
Fifteen years ago, at the 2008 Conference on Retroviruses and Opportunistic Infections (CROI), researchers announced that they had cured a patient – Timothy Ray Brown, initially known only as the Berlin Patient to preserve his privacy – of HIV through a hematopoietic stem cell transplant. Now, as researchers are gathered in Seattle for CROI 2023, reports of another cured patient were published Feb. 20, 2023, in Nature Medicine. Ten years after receiving a hematopoietic stem cell transplant, and 4 years after stopping antiretroviral treatment (ART), a 53-year-old patient may have been cured of HIV infection.
Results published Feb. 17, 2023, in Immunity have given a wider view of what happens in the earliest stages of HIV infection. Treatments against HIV prevent the replication of the virus, but do not kill the reservoir of latently infected cells that starts to build almost immediately upon infection.
In advanced or metastatic prostate cancer (PCa), patients may reach a stage where they do not respond to therapy. This stage is associated with chromosomal instability (CIN) and allow cells, up to a certain threshold, to adapt to therapy. However, a Mayo Clinic study has found a way to push that line so that cancer cells are so aberrant that they die.
Researchers from The Salk Institute have described a signaling pathway that sets off an unusual, autophagy-dependent cell death mechanism as a fail-safe for cells that have evaded senescence mechanisms. The scientists found a tumor suppression mechanism mediated by telomere signaling, which activated an innate immune response through mitochondrial and telomere complexes to eliminate cells with shortened telomeres.
An allogeneic hematopoietic stem cell transplantation that triggers graft-vs.-host-disease (GVHD) involves T cells that do not come from the patient's bloodstream, but rather from the local progenitor cells of the donor tissue. A study from the University of Pittsburgh confirmed this finding after cloning and following these cells, revealing their origin and peculiarities.
“I have had this idea for a pretty long time. In the tissues there are antigen-presenting cells and there are T cells. And I felt like there is no reason why they are needed to be input from blood that it could be a largely local response. Then, the question was whether there would be a subset of cells in the tissues that could continue to sustain it,” lead author Warren Shlomchik told BioWorld.
Treatment with the fusion protein QL-1005 reduced caloric intake and body weight in mice and primates. In obese animals, it also improved insulin, fasting glucose and triglyceride levels. The design belongs to the Chinese biopharmaceutical company Beijing QL Biopharmaceutical, which will begin clinical trials in a year.
Using a near-atomic resolution cryo-electron microscope and imaging techniques that prevent loss of information, scientists at the La Jolla Institute for Immunology (LJI) and Regeneron Pharmaceuticals Inc. have obtained the complete 3D structure of the glycoprotein of the Ebola virus and that of the drug that neutralizes it, Inmazeb, the first FDA-approved treatment for this deadly virus. “The challenge was embracing the inherent asymmetry, the heterogeneity that is really there in biology, understanding it and collecting enough data to get all the images without needing to force any symmetry averaging,” senior author Erica Ollmann Saphire told BioWorld.
The suppression of the SYF2 factor could be a new therapeutic strategy for the treatment of the different types of amyotrophic lateral sclerosis (ALS). According to a study from the University of Southern California, SYF2 acts on the TDP-43 protein, improving the survival of motor neurons affected by this disease. “We wanted to find something that would improve neuron survival across many different iPSC lines for ALS,” Justin Ichida told BioWorld.
The combination of two sequencing techniques has unveiled features of a subpopulation of cells that could be producing plaques in atherosclerosis. This process is associated with an autoimmune component driven by CD4+ T cells, according to a study from researchers at Leiden University.
