Pathogenesis of Viral Infections and Male Reproductive Health: An Evidence-Based Study.

Viruses, being intracellular obligate parasites, can cause several congenital and sexually transmitted diseases. Depending on the site of infection, viruses can adopt various pathogenic mechanisms for their survival and to escape the host immune response. The male reproductive system is one of the attainable targets of many viruses including immunodeficiency virus (HIV), Zika virus (ZIKV), adenovirus, cytomegalovirus (CMV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and infection with such viruses may cause serious health issues. Leydig cells and seminiferous tubules are the prime sites of mammalian testis for viral infection. The azoospermic condition is a common symptom of viral infection, wherein the hypothalamic-pituitary-testicular (HPT) axis can be disrupted, leading to decreased levels of luteinizing hormone (LH). Furthermore, oxidative stress (OS) is a major contributing factor to viral infection-associated male infertility. The likelihood of direct and indirect infection, as well as sex-based variability in the vulnerability pattern to viral infections, has been observed. However, there appears to be a long-term impact of viral infection on male reproductive performance due to testicular tissue pathogenicity - a process that requires thorough investigation. The present study aimed to explore how the viruses affect the male reproductive system, including their distribution in tissues and body fluids, possible targets as well as the effects on the endocrine system. We used the major electronic databases such as MEDLINE and SCOPUS. Google Scholar was also consulted for additional literature search related to the topic. Obtained literatures were sorted based on the content. The articles that reported the pathogenesis of viruses on male reproductive health and were published in the English language were included in the present study.

A new era of radiation resistance bacteria in bioremediation and production of bioactive compounds with therapeutic potential and other aspects: An in-perspective review.

Microorganisms that survive in extreme environmental conditions are known as 'extremophiles'. Recently, extremophiles draw an impression in biotechnology/pharmaceutical researches/industries because of their novel molecules, known as 'extremolytes'. The intriguing phenomenon of microbial radiation resistance probably arose independently throughout their evolution of selective pressures (e.g. UV, X-ray, Gamma radiation etc.). Radiation produces multiple types of damage/oxidation to nucleic acids, proteins and other crucial cellular components. Most of the literature on microbial radiation resistance is based on acute γ-irradiation experiments performed in the laboratory, typically involving pure cultures isolation and their application on bioremediation/therapeutic field. There is much less information other than bioremediation and therapeutic application of such promising microbes we called as 'new era'. Here we discus origin and diversity of radiation resistance bacteria as well as selective mechanisms by which microorganisms can sustain in radiation rich environment. Potential uses of these radiations resistant microbes in the field of bioremediation, bioactive compounds and therapeutic industry. Last but not the least, which is the new aspect of radiation resistance microbes. Our review suggest that resistance to chronic radiation is not limited to rare specialized strains from extreme environments, but can occur among common microbial taxa, perhaps due to overlap molecular mechanisms of resistance to radiation and other stressors. These stress tolerance potential make them potential for radionuclides remediation, their extremolytes can be useful as anti-oxidant and anti-proliferative agents. In current scenario they can be useful in various fields from natural dye synthesis to nanoparticles production and anti-cancer treatment.

Dynamic modularity of host protein interaction networks in Salmonella Typhi infection.

BACKGROUND: Salmonella Typhi is a human-restricted pathogen, which causes typhoid fever and remains a global health problem in the developing countries. Although previously reported host expression datasets had identified putative biomarkers and therapeutic targets of typhoid fever, the underlying molecular mechanism of pathogenesis remains incompletely understood. METHODS: We used five gene expression datasets of human peripheral blood from patients suffering from S. Typhi or other bacteremic infections or non-infectious disease like leukemia. The expression datasets were merged into human protein interaction network (PIN) and the expression correlation between the hubs and their interacting proteins was measured by calculating Pearson Correlation Coefficient (PCC) values. The differences in the average PCC for each hub between the disease states and their respective controls were calculated for studied datasets. The individual hubs and their interactors with expression, PCC and average PCC values were treated as dynamic subnetworks. The hubs that showed unique trends of alterations specific to S. Typhi infection were identified. RESULTS: We identified S. Typhi infection-specific dynamic subnetworks of the host, which involve 81 hubs and 1343 interactions. The major enriched GO biological process terms in the identified subnetworks were regulation of apoptosis and biological adhesions, while the enriched pathways include cytokine signalling in the immune system and downstream TCR signalling. The dynamic nature of the hubs CCR1, IRS2 and PRKCA with their interactors was studied in detail. The difference in the dynamics of the subnetworks specific to S. Typhi infection suggests a potential molecular model of typhoid fever. CONCLUSIONS: Hubs and their interactors of the S. Typhi infection-specific dynamic subnetworks carrying distinct PCC values compared with the non-typhoid and other disease conditions reveal new insight into the pathogenesis of S. Typhi.