BackgroundFemale prisoners are at risk of acquiring sexually transmitted infections (STIs). There has been no previous study regarding the epidemiological status of STIs among female prisoners in Isfahan, central Iran.ObjectivesThe aim of this study was to investigate the prevalence and risk factors of the aforementioned infections among women incarcerated in the central prison, Isfahan, to determine appropriate prevention measures.Patients and MethodsIn a cross-sectional study, all of the 163 women incarcerated in the central prison, Isfahan in 2009, were voluntarily enrolled by the census method. After completing a checklist consisting of demographic, social, and risk factors, a 5ml blood sample was taken from each individual. The sera were analyzed for markers of the hepatitis B virus (HBV; HBsAg, HBsAb, HBcAb), hepatitis C virus (HCV; HCV antibodies), human immunodeficiency virus (HIV; HIV antibodies), and syphilis (RPR). Confirmatory tests were performed on HCV antibody-positive cases.ResultsThe mean age of the participants in the study was 34.54 ± 11.2 years old, 94.3% of these women were Iranian, and many of them had only a primary level of education. The prevalence of HBsAg, HBcAb, HBsAb, and HCV antibodies were; 1.2%, 7.4%, 12.9% and 7.4% respectively. No positive RPR or HIV antibodies were detected.ConclusionsA significant relationship was seen between the HCV antibody, drug injection and illegal sex in the women, and also between HBc-Ab and drug injection. Regular screening, educational programs, and facilitation of access to suitable treatment care should be widely implemented in the prison population. Testing for immunity against HBV should be considered on admission, and afterwards vaccination of all prisoners and an appropriate preventative approach should be applied.

The emerging new Coronaviridae member, nCoV 19, outbreak announced a pandemic by WHO with an increased morbidity and mortality rate worldwide. nCoV 19 known as the third highly pathogen coronavirus in the human population after the severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV), the nCoV 19. The renin-angiotensin (RAS) signaling pathway, oxidative stress and cell death, cytokines storm and endothelial dysfunction are four major pathways involved in the pathogenesis of nCoV 19. Acute respiratory distress syndrome (ARDS) generally develops with a massive oxidative/nitrosative stress following virus entry and RAS activation. The DNA damage subsequent to oxidative burst activates poly-ADP ribose polymerase-1 (PARP-1), viral macrodomain (NSP3) poly (ADP-ribose) glycohydrolase (PARG) and transient receptor potential channel, melastatin 2 (TRPM2) in a sequential manner ultimately leading to apoptosis and necrosis due to NAD and ATP depletion. Regarding the molecular mechanisms involved in nCoV 19 pathogenesis, angiotensin II receptor blockers and/or PARP, PARG and TRPM2 blockers could be engaged as therapeutic candidates for inhibition of RAS and quenching oxidative stress, respectively. In this review, the molecular aspects of nCoV 19 pathogenesis would be studied precisely and possible therapeutic targets would be proposed. It is recommended to evaluate the proposed drugs and supplements via registered clinical trials along with conventional guideline-based multi-drug regimen.

In late 2019, a new member of the Coronaviridae family, officially designated as “severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2), emerged and spread rapidly. The Coronavirus Disease-19 (COVID-19) outbreak was accompanied by a high rate of morbidity and mortality worldwide and was declared a pandemic by the World Health Organization in March 2020. Within the Coronaviridae family, SARS-CoV-2 is considered to be the third most highly pathogenic virus that infects humans, following the severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV). Four major mechanisms are thought to be involved in COVID-19 pathogenesis, including the activation of the renin-angiotensin system (RAS) signaling pathway, oxidative stress and cell death, cytokine storm, and endothelial dysfunction. Following virus entry and RAS activation, acute respiratory distress syndrome develops with an oxidative/nitrosative burst. The DNA damage induced by oxidative stress activates poly ADP-ribose polymerase-1 (PARP-1), viral macrodomain of non-structural protein 3, poly (ADP-ribose) glycohydrolase (PARG), and transient receptor potential melastatin type 2 (TRPM2) channel in a sequential manner which results in cell apoptosis or necrosis. In this review, blockers of angiotensin II receptor and/or PARP, PARG, and TRPM2, including vitamin D3, trehalose, tannins, flufenamic and mefenamic acid, and losartan, have been investigated for inhibiting RAS activation and quenching oxidative burst. Moreover, the application of organic and inorganic nanoparticles, including liposomes, dendrimers, quantum dots, and iron oxides, as therapeutic agents for SARS-CoV-2 were fully reviewed. In the present review, the clinical manifestations of COVID-19 are explained by focusing on molecular mechanisms. Potential therapeutic targets, including the RAS signaling pathway, PARP, PARG, and TRPM2, are also discussed in depth.

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