Cytomegalovirus Reactivation in Patients With Acute Lymphoblastic Leukemia in Non-transplant Setting

Abbas, Mansoor; Naeem, Sameen Bin; Jhatial, Mussadique Ali; Bokhari, Syed W; Ahsan, Bushra; Ahmad, Usman

doi:10.7759/cureus.32936

Cited by 1 publication

(1 citation statement)

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“…Monocytes serve as viral vehicles responsible for the hematogenous dissemination of the pathogen. Monocyte-derived macrophages may be either the sites of productive infection or the pathogen reservoirs in the host tissues [82][83][84][85][86].…”

Section: Mcl-1 In Hcmv Infectionmentioning

confidence: 99%

Mcl-1 Protein and Viral Infections: A Narrative Review

Wyżewski,

Stępkowska,

Kobylińska

et al. 2024

IJMS

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MCL-1 is the prosurvival member of the Bcl-2 family. It prevents the induction of mitochondria-dependent apoptosis. The molecular mechanisms dictating the host cell viability gain importance in the context of viral infections. The premature apoptosis of infected cells could interrupt the pathogen replication cycle. On the other hand, cell death following the effective assembly of progeny particles may facilitate virus dissemination. Thus, various viruses can interfere with the apoptosis regulation network to their advantage. Research has shown that viral infections affect the intracellular amount of MCL-1 to modify the apoptotic potential of infected cells, fitting it to the “schedule” of the replication cycle. A growing body of evidence suggests that the virus-dependent deregulation of the MCL-1 level may contribute to several virus-driven diseases. In this work, we have described the role of MCL-1 in infections caused by various viruses. We have also presented a list of promising antiviral agents targeting the MCL-1 protein. The discussed results indicate targeted interventions addressing anti-apoptotic MCL1 as a new therapeutic strategy for cancers as well as other diseases. The investigation of the cellular and molecular mechanisms involved in viral infections engaging MCL1 may contribute to a better understanding of the regulation of cell death and survival balance.

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