Unraveling The Impact of Viral Infections on Sperm Genetic Stability: A Scoping Review

Abstract

Despite the apparent resilience of the male reproductive system, various viruses have been found to impact male fertility by causing testicular inflammation, hormonal imbalances, and sperm abnormalities. The integrity of the genome is vital for cell function, and its instability, influenced by various factors including viral infections, may contribute to age-related conditions such as cancer and neurodegenerative disorders. This scoping review aims to investigate the relationship between viral infections and sperm genetic stability, exploring their interactions and potential impact on male reproductive health and fertility. In order to conduct this scoping review, PubMed, MEDLINE (OVID), ScienceDirect, Google Scholar, and Cochrane databases were explored to find the relevant articles using a search strategy developed in collaboration with a medical librarian. Two independent reviewers screened titles and abstracts of the relevant papers, followed by full-text screening. Studies focusing on infertile males with viral infections, compared to fertile males, examining DNA damage and sperm abnormalities were included. Thirty-four studies were included in the current review. This review will provide valuable information to healthcare professionals in addressing virusinduced sperm genetic instability and its implications for reproductive health. Furthermore, it highlights the socioeconomic and public health aspects of preventing and managing viral infections.

Keywords: Chromosomal Abnormalities; DNA Damage; Male Infertility; Spermatozoa; Viral Infection.

Fig 1

Flowchart representing the study selection steps.

Fig 2

This cascade of events highlights the complex and destructive nature of the relationship between ROS, inflammation, apoptosis, DFI and genome instability in the context of viral infections and their impact on male reproductive health. Viral infections induce an upregulation of proinflammatory cytokines. ROS contribute to lipid peroxidation by attacking polyunsaturated fatty acids in the plasma membrane, while also initiating DNA fragmentation and apoptosis in both testes and sperm cells. The released cytokines further exacerbate the situation ultimately leading to diminished sperm parameters and increased sperm chromosomal instability/ abnormality. ROS; Reactive oxygen species, DFI: DNA fragmentation index, HPV; Human papillomavirus, HBV; Hepatitis B virus, HSV; Herpes simplex virus, EBV; EpsteinBarr virus, HCMV; Human cytomegalovirus, HHV; Human herpesvirus, HIV; Human immunodeficiency virus, HCV; Hepatitis C virus, ZIKV; Zika virus, and SARS-CoV; Severe acute respiratory syndrome coronavirus.

Fig 3

Viral genes integration into the host genome and transmission of genetic material. A. Some DNA viruses reversibly attach to the host cell surface proteoglycans with a low affinity; this is followed by the process involving more specific receptor(s) with high affinity to mediate the early entry step; and after endocytosis-mediated internalization, the virus fuses with the cellular membrane compartment, probably in an endosomal compartment. The nucleocapsid is transported to the nucleus, and then integrated into the host genome. B. Some viruses have an RNA genome. After the virus enters a cell, the viral enzyme reverse transcriptase copies the RNA into a linear cDNA. The viral cDNA moves to the nucleus where integrase catalyzes the covalent joining of the viral cDNA genome to the host DNA. The integrated viral genome is called the provirus. After integration in either way, the viral genome is transcribed and translated by host machinery to generate progeny viruses.