Anti-A33 Antibodies May Hold the Keys to Effective Therapy against Poxvirus Infections Including Monkeypox

Like many other viruses, the poxvirus is a killer virus that has been implicated in quite a number of diseases. While a disease such as smallpox caused by this organism is obsolete, another, like the relatively novel monkeypox is still pestilent. In fact, according to the World Health Organization WHO, there have been a total of 92 confirmed monkeypox cases in less than ten days (between May 13th and May 21st, 2022) in places initially thought to be non-endemic, including the United States, Portugal, France, and Canada.

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Stages of Monkeypox

Stages of Monkeypox. Credit: UK government

Effective therapy for the poxvirus has continued to elude scientists majorly because a complete or at least significant understanding of this organism sufficient for developing one has not yet been achieved. And although there are vaccines against smallpox, a cure for the disease is yet to be discovered. However, in a study conducted by scientists and funded by the National Natural Science Foundation of China, a new approach to therapy for poxvirus-caused diseases was theorized. This approach relied on anti-A33 antibodies against poxvirus.

Role of anti-A33 antibodies in efficient poxvirus therapy

Anti-A33 antibodies are proteins found on the protein coat (or capsid) which encloses the poxvirus DNA genome. The capsid acts as a protective shell for the virus’s genetic material. However, although this protein coat protects, it may sometimes form the basis of vaccination developed against certain viruses. For instance, the A33 antigen on the protein coat of the vaccinia virus (which causes smallpox-like symptoms) is used to develop vaccines against smallpox. Here, the vaccinia virus bearing this antigen is introduced into the person. In response to the foreign invader, the person’s immune system produces active B cells which immediately destroy the antigen, and also memory B cells with the ability to easily recognize and effectively destroy any virus bearing this antigen in the future.

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The memory B cell-specific against the A33 protein was an important factor in this study. Using multi-fluorescence-labeled tetrameric A33 antigen, the scientists effectively located the rare poxvirus-specific memory B cells from PMCB of volunteers with vaccinia virus immunization more than 40 years ago. After isolating these cells, the DNA responsible for coding the antibodies was identified using ‘reverse transcription.’ Finally, using real-time polymerase chain reaction PCR, the expression of these genes was analyzed.

The result of this analysis showed that the H2 antibody showed a relatively high affinity and specificity for the A33 antigen. The antibody effectively inhibited viral infections and spread in cells.

When passive immunotherapy of H2 was carried out in mice either prophylactically to present poxvirus infections or therapeutically to treat an already existing illness, the therapy proved to be very effective.

Clinical significance

These results suggest the potential of the anti-A33 human antibody-based detection and therapeutics for poxvirus infection. Therapy that mimics the action of H2 could be used to detect and treat diseases caused by this virus. Also, increasing the expression of the H2 gene may form an alternative treatment for patients with monkeypox.

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Conclusion

Monkeypox may just be the next worldwide pandemic after COVID. This study hints at a cure for diseases such as monkeypox way before any future global outbreaks.

References

Protective human anti-poxvirus monoclonal antibodies are generated from rare memory B cells isolated by multicolor antigen tetramers

Multi-country monkeypox outbreak in non-endemic countries

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