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• W4362659012 abstract "Dear Editor, Monkeypox is an infectious zoonotic disease which is caused by monkeypox virus. It belongs to the genus Orthopoxvirus and the family Poxviridae. The lethality rate of this disease ranges from 1 to 10%. The first occurrence of this disease was in the Democratic Republic of the Congo, Africa. Monkeypox spreads mainly through direct contact with body fluids, respiratory droplets of infected patients and through animals who act as its reservoir The genome of monkeypox virus is linear, enveloped, and double-stranded DNA1,2. This disease mainly has two phases, the first one is the invasive phase which is characterized mainly by fatigue, sore throat, fever, and myalgia. The second phase is the eruptive phase which is characterized by the clinical symptoms of pustular lesions on the legs, multiple lesions on the penile sulcus and huge ulcerative lesions on the perianal skin3. In the current decade, extracellular vesicles (EVs) have gained much attention due to their ability that leads to intercellular communication by activation of various cell signalling pathways. Tetraspanins are the group of surface EVs protein which involved viral particles associated with targeting cells and fission with the recipient cells via cellular membranes. Virus-derived EVs internal cargo influence the recipient cell activity. Envelop virus and EVs have biologically active cargo transportation ability4. EVs are released for normal or pathological conditions (it may be cancer cells or viral-infected cells). The origin of EVs is different as exosomes develop from the plasma membrane and apoptotic bodies develop during the apoptosis process, microvesicles secrete from the plasma membrane and endoplasmic reticulum (these are three major subpopulations of EVs). EVs regulate host–pathogen cellular communication. Viral-infected cell-derived EVs mediated protein and nucleic acid (DNA, RNA) transportation promote the viral pathogenesis progression5,6. In the context of viral infections, the biological role of EVs might have two opposing effects. EVs can influence recipient cells based boosting viral reproduction on the one hand, or they can prevent viral replication by inducing host immune responses on the other7. In addition, integrating viral proteins can cause nonparticipating immune cells to die, which would contribute to the significant loss of immune cells during the initial phases of viral infection or when the viral load is low. In addition to making immune cells more Susceptible to viral infection, intercellular transfer of viral proteins and viral cell surface receptors by EVs aids in evading the host’s immunological response by reducing lymphocyte synthesis of antibodies8. The aim of the article is to highlighted the EVs’ interrelation with the virus and encourage large-scale virologists to decode the virus and EVs related to several aspect. Ethical approval None. Sources of funding None. Authors’ contribution D.M., B.B., R.D., S.N., and P.S.: conceptualization, study design, and writing. A.D. and S.K.J.: editing and reviewing. Conflicts of interest disclosure The authors declare that they have no financial conflict of interest with regard to the content of this report. Research registration unique identifying number (UIN) None. Guarantor Saurabh K. Jha." @default.
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• W4362659012 date "2023-03-01" @default.
• W4362659012 modified "2023-10-17" @default.
• W4362659012 title "Monkeypox and extracellular vesicles interlink: an unexplored chapter" @default.
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• W4362659012 doi "https://doi.org/10.1097/js9.0000000000000069" @default.
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