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| LETTER TO EDITOR |
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| Year : 2022 | Volume
: 66
| Issue : 3 | Page : 384-385 |
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Monkeypox virus - Immune imprinting
Sathish Sankar
Professor, Department of Microbiology, Saveetha Dental College and Hospitals, Chennai, Tamil Nadu, India
| Date of Submission | 27-Jun-2022 |
| Date of Decision | 29-Jul-2022 |
| Date of Acceptance | 03-Aug-2022 |
| Date of Web Publication | 22-Sep-2022 |
Correspondence Address:
Sathish Sankar
Department of Microbiology, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Chennai - 600 077, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijph.ijph_848_22
How to cite this article:
Sankar S. Monkeypox virus - Immune imprinting. Indian J Public Health 2022;66:384-5 |
Dear Editor,
Monkeypox virus is an enveloped double-stranded DNA virus belonging to the Orthopoxvirus of Poxviridae. First isolated and identified in 1958 in monkeys and 1970 in humans, causes viral zoonotic infection similar to smallpox.[1] The disease is endemic to West and Central Africa and spread to other countries in recent years. Although the epidemic risk for humans is small, the repeating virus circulation, especially among immunosuppressed could promote viral evolution and re-emergence with high transmissibility and severity.[2]
Immune imprinting is now widely studied for many vaccine-preventable viral infections. The term is defined as a phenomenon when an initial exposure is confined to the activated B-cell memory to one virus strain and limiting from producing memory B-cells and neutralizing antibodies against other novel viral variants. The influenza A virus vaccine provides an imprinted immune response to the previous strains providing limited neutralizing antibodies against new strains. Similar immune imprinting was evidenced recently with SARS-CoV-2 infection. People exposed to the different variants of the virus during the COVID-19 pandemic elicit variant-specific antibodies. However, due to immune imprinting with the primary response to ancestral strain, the immune response wanes to other variants of the same pathogen. Immune response depending on previous exposure is imprinted that determines the variant recognition and protection [Figure 1]. This explains different patterns of immunity among individuals, the recent infection surge with BA.5 variant and the inability of the mRNA and other vaccines to prevent breakthrough infection and reinfection.[3],[4],[5] Many factors influence immune imprinting and result in neutralization escape with the emergence of new variants. The understanding of the phenomenon is thus important to counter new variants and design effective vaccines. | Figure 1: Immune imprinting in viral infections. Note: The picture is drawn by the author.
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Increase in population, accumulation of unvaccinated cohorts, and waning immunity to smallpox and other factors pose the risk of monkeypox infection.[6] The sequences of central coding regions are highly conserved among orthopox viruses. The genome of the monkeypox virus differs from the vaccinia virus in possessing four open reading frames in the inverted terminal-inverted repeats. The role of negative selection-driven gene loss in favoring the virus adaptation leading to disease emergence with higher transmissibility and pathogenicity has not been studied.[7] The codon usage indices of the monkeypox genome indicate synonymous codon usage bias and mutational pressure balanced with selection pressure. Although mutations in the monkeypox genome occur much lower, the evolutionary mutation rate and the consequent emergence of new strains of circulating monkeypox viruses remain elusive.
Vaccinia virus vaccine for smallpox confers 85% immunity to monkeypox virus infection and the neutralizing antibody and total IgG persists for several decades. The information on the circulating monkeypox virus strains and neutralizing ability of the preexisting immune response to smallpox virus that could confer immunity to the monkeypox virus is limited.
Data on current serological immunity are scarce and preparedness for the possible bioterrorism threat is limited, especially in vulnerable countries such as India. Further studies on the immune status against smallpox, especially among the susceptible population could help prepare for the management in the event of re-emerging smallpox and devise strategies to encounter monkeypox viral infection.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
 References | |  |
| 1. | Bunge EM, Hoet B, Chen L, Lienert F, Weidenthaler H, Baer LR, et al. The changing epidemiology of human monkeypox-A potential threat? A systematic review. PLoS Negl Trop Dis 2022;16:e0010141.  |
| 2. | Grant R, Nguyen LL, Breban R. Modelling human-to-human transmission of monkeypox. Bull World Health Organ 2020;98:638-40. |
| 3. | Röltgen K, Nielsen SC, Silva O, Younes SF, Zaslavsky M, Costales C, et al. Immune imprinting, breadth of variant recognition, and germinal center response in human SARS-CoV-2 infection and vaccination. Cell 2022;185:1025-40.e14. |
| 4. | Reynolds CJ, Pade C, Gibbons JM, Otter AD, Lin KM, Muñoz Sandoval D, et al. Immune boosting by B.1.1.529 (Omicron) depends on previous SARS-CoV-2 exposure. Science 2022;377:eabq1841. |
| 5. | Wheatley AK, Fox A, Tan HX, Juno JA, Davenport MP, Subbarao K, et al. Immune imprinting and SARS-CoV-2 vaccine design. Trends Immunol 2021;42:956-9. |
| 6. | Nguyen PY, Ajisegiri WS, Costantino V, Chughtai AA, MacIntyre CR. Reemergence of human monkeypox and declining population immunity in the context of Urbanization, Nigeria, 2017-2020. Emerg Infect Dis 2021;27:1007-14. |
| 7. | Kugelman JR, Johnston SC, Mulembakani PM, Kisalu N, Lee MS, Koroleva G, et al. Genomic variability of monkeypox virus among humans, Democratic Republic of the Congo. Emerg Infect Dis 2014;20:232-9. |
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