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Review
. 2025 Feb 2;14(2):134.
doi: 10.3390/pathogens14020134.

Merkel Cell Polyomavirus Co-Infection in HIV/AIDS Individuals: Clinical Diagnosis, Consequences and Treatments

Affiliations
Review

Merkel Cell Polyomavirus Co-Infection in HIV/AIDS Individuals: Clinical Diagnosis, Consequences and Treatments

Xianfeng Zhou et al. Pathogens. .

Abstract

Merkel cell polyomavirus (MCV) was named for its role as the causative agent of Merkel cell carcinoma (MCC), which is MCV positive in approximately 80% of cases. MCV is classified as a Group 2A carcinogen, which promotes carcinogenesis by integrating T-antigen into the cell genome. The prevalence of anti-MCV antibodies in the general population can be as high as 90%. MCV typically promotes cancer by integrating T-antigen genes into the host cell genome, and 80% of MCC cases are attributed to MCV activation. In immunocompetent individuals, MCV usually remains latent after infection. However, the incidence of MCC increases significantly in immunocompromised or immunodeficient patients, such as those who have undergone organ transplantation, have chronic lymphocytic leukemia, or are living with human immunodeficiency virus (HIV) infection. Acquired immunodeficiency is a particular feature of people living with HIV. Currently, research on HIV/AIDS patients with MCV infection, clinical outcomes, and treatments is quite limited. This paper reviews previous research and systematically examines the relationship between HIV/AIDS and MCV-associated diseases, with the aim of providing valuable information for the prevention, diagnosis, and treatment of MCV in vulnerable populations.

Keywords: HIV/AIDS; Merkel cell carcinoma; Merkel cell polyomavirus; activation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The double-stranded DNA of MCV is divided into three functional regions: early region (EVGR), late region (LVGR), and intermediate non-coding control region (NCCR), which contains bidirectional promoters and virus replication origin (A); the EVGR (196ȁ3080 nt) includes early region genes of LT, ST, 57 kT, and MCV-miR-M1 (B); Linear diagram of MCV genome for LT, sT, and ALTO (C). PP2A, protein phosphatase 2A; RB, retinoblastoma.
Figure 2
Figure 2
Diagram of HIV infection that causes CD4+ T cells decline and HIV life cycle in CD4+ T cell.
Figure 3
Figure 3
Diagram of risk factors, clinical diagnosis, vulnerable populations, and recommended treatments of MCC. Clinical diagnosis with the “AEIOU” principle and treatments recommended are listed for MCC. MCC mainly occurs in UV-exposed sites including face, limbs, hands, eyelids, etc. Given the complexity, invasiveness, and individual differences of each case, MCC is best treated by a multidisciplinary team.
Figure 4
Figure 4
Principles of systematic therapy of MCC under the NCCN guidelines (Version 1.2023). N0: no regional lymph node metastasis detected on clinical and/or radiologic examination; N+: regional lymph nodes cannot be clinically assessed (e.g., previously removed for another reason, or because of body habitus); M1: distant metastasis detected on clinical and/or radiologic examination; RT: radiation therapy.

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