MVA-B

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MVA-B, or Modified Vaccinia Ankara B, is an

HIV subtype in Europe".[1] It has been stated by Dr. Esteban that, in the future, the vaccine could potentially reduce the virulence of HIV to a "minor chronic infection akin to herpes".[2]

History

Non-human testing

The vaccine was originally tested on a number of mice and macaque monkeys in 2008 against the Simian immunodeficiency virus (SIV) and it was found to be successful in creating an immune system response to SIV infection.[1][3]

Phase I testing

The initial testing on human subjects was conducted on a testing pool of thirty HIV-free individuals. Six of the pool were given a

CD4+ T lymphocytes and CD8+ T lymphocytes were at 38.5% and 69.2% each for the testers given the vaccine, while the amounts in the group given the placebo remained at 0%.[3][4]

The next step with the vaccine within Phase I testing is to conduct a trial with HIV-positive testers, in order to determine if there is a "therapeutical effect of the vaccine" on those already infected with the virus.[1] A randomized controlled trial was published in February of 2015 that involved 30 HIV infected patients, 20 given doses of MVA-B and 10 given a placebo, which showed that the vaccine was capable of increasing T cell response for Gag-specific T cells. This, however, did not improve immune responses in the long run or prevention of resurgence of viral loads after vaccine treatment was concluded.[5] A followup study published in October of 2017 showed that subsequent immunization with the vaccine in HIV positive patients that had received MVA-B four years prior saw a larger immune response and production of binding and neutralizing antibodies to HIV replication.[6]

Virology

In order to create the vaccine, researchers took the prior Modified Vaccinia Ankara virus and added four

genes from the HIV genome, specifically those titled Gag, Pol, Nef and Env.[1] An improved version of the recombinant viral vector, which was titled MVA-B ΔA40R, was created and published in February of 2020 that included a deletion of the A40R gene in the vaccine genome. It is unknown what function the A40 protein has, other than it causing protein accumulation in the cell membrane, but deletion of it resulted in a vaccine that boosted transcription and expression levels of interferon (IFN)-β, IFN-induced genes, and chemokines in exposed macrophages.[7]

See also

  • Antiretroviral drug

References

  1. ^ a b c d e Jesus Diaz (September 28, 2011). "This 90 Percent Successful Vaccine May Be Our Best Chance to Eradicate AIDS". Gizmodo. Retrieved September 29, 2011.
  2. ^ Stephen Adams (September 29, 2011). "HIV could be 'minor infection' with new vaccine". Irish Independent. Retrieved September 29, 2011.
  3. ^ a b Gopalan T (September 28, 2011). "Promising Show By HIV Vaccine MVA-B In Clinical Trials". Medindia. Retrieved September 29, 2011.
  4. ^ Ylva Mossing (September 29, 2011). "Vaccin gör HIV till "mindre infektion"". Aftonbladet (in Swedish). Retrieved September 29, 2011.
  5. PMID 25724985
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Further reading

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