Pathophysiological and molecular considerations of viral and bacterial infections during maternal-fetal and –neonatal interactions of SARS-CoV-2, Zika, and Mycoplasma infectious diseases

Abstract

During pregnancy, a series of physiological changes are determined at the molecular, cellular and macroscopic level that make the mother and fetus more susceptible to certain viral and bacterial infections, especially the infections in this and the companion review. Particular situations increase susceptibility to infection in neonates. The enhanced susceptibility to certain infections increases the risk of developing particular diseases that can progress to become morbidly severe. For example, during the current pandemic caused by the SARS-CoV-2 virus, epidemiological studies have established that pregnant women with COVID-19 disease are more likely to be hospitalized. However, the risk for intensive care unit admission and mechanical ventilation is not increased compared with nonpregnant women. Although much remains unknown with this particular infection, the elevated risk of progression during pregnancy towards more severe manifestations of COVID-19 disease is not associated with an increased risk of death. In addition, the epidemiological data available in neonates suggest that their risk of acquiring COVID-19 is low compared with infants (<12 months of age). However, they might be at higher risk for progression to severe COVID-19 disease compared with older children. The data on clinical presentation and disease severity among neonates are limited and based on case reports and small case series. It is well documented the importance of the Zika virus infection as the main cause of several congenital anomalies and birth defects such as microcephaly, and also adverse pregnancy outcomes. Mycoplasma infections also increase adverse pregnancy outcomes. This review will focus on the molecular, pathophysiological and biophysical characteristics of the mother/placental-fetal/neonatal interactions and the possible mechanisms of these pathogens (SARS-CoV-2, ZIKV, and Mycoplasmas) for promoting disease at this level.

Mycoplasmas as Host Pantropic and Specific Pathogens: Clinical Implications, Gene Transfer, Virulence Factors, and Future Perspectives

“…The 16S rRNA gene sequencing was also carried out which showed 99% nucleotide identity to M. hominis (Kersin et al, 2020). M. hominis is characterized by a very slow growth rate that requires specific growth media and it's resistant to many antibiotics such as b-lactams, glycopeptides, sulfonamides, and macrolides (Kersin et al, 2020;Ferreira et al, 2022).…”

COVID-19 pandemic: A multidisciplinary perspective on the pathogenesis of a novel coronavirus from infection, immunity and pathological responses

“…The consensus achieved by the current study is that the entry and spread of the SARS-CoV-2 virus depend on the host ACE2 receptor and the serine protease TMPRSS2, with possible involvement of B/L7 and furin proteases (27).…”

“…And laboratory studies have shown that its antiviral effects are attributed to multiple mechanisms, including fighting coronavirus infection by blocking the glycosylation of host receptors (23,24), inhibiting the processing of S proteins, and suppressing the inflammatory response (25). ACE2 (27). Accordingly, it has been found that tetracycline and doxycycline can act as inhibitors of ACE2-peg binding (28).…”

Extracellular HMGB1 as Inflammatory Mediator in the Progression of Mycoplasma Gallisepticum Infection

“…A key characteristic of pathogenic mycoplasma that interferes with the host response is its ability to alter the secretion of immunomodulatory substances [ 14 ]. Mycoplasma gallisepticum (MG), a major pathogenic microorganism causing chronic respiratory disease (CRD) in chickens, persistently triggers the release of immune factors after infection of the host to maintain chronic inflammation [ 15 , 16 , 17 ].…”