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Scientists have engineered a "tri-specific antibody" that they say can attack 99% of HIV strains:
Scientists have engineered an antibody that attacks 99% of HIV strains and can prevent infection in primates. It is built to attack three critical parts of the virus - making it harder for HIV to resist its effects.
The work is a collaboration between the US National Institutes of Health and the pharmaceutical company Sanofi. The International Aids Society said it was an "exciting breakthrough". Human trials will start in 2018 to see if it can prevent or treat infection.
Trispecific broadly neutralizing HIV antibodies mediate potent SHIV protection in macaques (DOI: 10.1126/science.aan8630) (DX)
The development of an effective AIDS vaccine has been challenging due to viral genetic diversity and the difficulty in generating broadly neutralizing antibodies (bnAbs). Here, we engineered trispecific antibodies (Abs) that allow a single molecule to interact with three independent HIV-1 envelope determinants: 1) the CD4 binding site, 2) the membrane proximal external region (MPER) and 3) the V1V2 glycan site. Trispecific Abs exhibited higher potency and breadth than any previously described single bnAb, showed pharmacokinetics similar to human bnAbs, and conferred complete immunity against a mixture of SHIVs in non-human primates (NHP) in contrast to single bnAbs. Trispecific Abs thus constitute a platform to engage multiple therapeutic targets through a single protein, and could be applicable for diverse diseases, including infections, cancer and autoimmunity.
(Score: 4, Interesting) by Chrontius on Saturday September 23 2017, @10:35PM
On the other hand, those viral strains that have adapted to evade the existing trispecific antibodies could also be targeted by their own monoclonal antibodies, perhaps given as a supplement to the HIV vaccine, conventional HAART, PREP to prevent infection, and that ignores the most important effect: It's now torn between evading the monoclonal antibody, and evading the human immune system. By selecting for those strains that evade the trispecific antibody, there is an opportunity cost - the virus could become less effective at entering cells, or more easily detected by the immune system, or produce fewer viral copies because of the energetic cost of building a less-efficient transmembrane protein kills the host cell more quickly, and many viral particles are released unfinished, therefore ultimately lowering the viral load. And HIV is, initially, held at bay by the immune system before the exponential replication hits an inflection point. Perhaps this strain of HIV isn't ever capable of bringing the viral load to that inflection point, and becomes a long-lasting but ultimately acute condition following a course like mononucleosis - you feel like shit for a couple months, then get better.
Science is complicated.