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      Men and COVID-19: A Pathophysiologic Review

      , MD 1 , 2 , , PhD, MED, MSTAT, MSIS, MBA 1 , 3 , 4 , 5

      American Journal of Men's Health

      SAGE Publications

      Men, COVID-19, SAR-CoV-2, coronavirus, pandemic, crisis, pathology, public health

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          Abstract

          Coronaviruses are single-stranded ribonucleic acid viruses that can cause illnesses in humans ranging from the common cold to severe respiratory disease and even death.In March 2020, the World Health Organization declared the 2019 novel coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as the first pandemic. Compared to women, most countries with available data report that men with COVID-19 have greater disease severity and higher mortality. Lab and animal data indicate that men respond differently to the SARS-CoV-2 infection, offering possible explanations for the epidemiologic observations. The plausible theories underlying these observations include sex-related differences in angiotensin-converting enzyme 2 receptors, immune function, hormones, habits, and coinfection rates.In this review we examine these factors and explore the rationale as to how each may impact COVID-19. Understanding why men are more likely to experience severe disease can help in developing effective treatments, public health policies, and targeted strategies such as early recognition and aggressive testing in subgroups.

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          Most cited references 27

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          The X-files in immunity: sex-based differences predispose immune responses

          Sex-based differences in immune responses can influence the susceptibility to autoimmune and infectious diseases and the efficacy of therapeutic drugs. In this Perspective, Eleanor Fish discusses factors, such as X-linked genes, hormones and societal context, that underlie disparate immune responses in men and women.
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            Masculinity and perceived normative health behaviors as predictors of men's health behaviors.

            This study examined the unique contributions of masculinity and men's perceptions of the normativeness of men's and women's health behaviors in predicting men's self-reported health behaviors. One hundred and forty men aged 18-78 were recruited from 27 unmoderated and moderated Internet listservs of potential interest to men. They completed measures on-line assessing masculinity, their perceptions of normative health behaviors for men and women, and 8 health behaviors (i.e., alcohol abuse, seatbelt use, tobacco use, physical fighting, use of social support, exercise, dietary habits, and receipt of annual medical check-ups). Findings suggest that masculinity and the perceived normativeness of other men's health behaviors significantly predicted participants' own health behaviors beyond that accounted for by socio-demographic variables (e.g., education, income). Perceptions of the normativeness of women's health behaviors were unrelated to participants' health behaviors. The findings support previous research which has found that traditional masculine gender socialization and social norms models encourage men to put their health at risk, and suggest directions for health promotion efforts when working with men.
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              Is Open Access

              The X chromosome and sex-specific effects in infectious disease susceptibility

              The X chromosome and X-linked variants have largely been ignored in genome-wide and candidate association studies of infectious diseases due to the complexity of statistical analysis of the X chromosome. This exclusion is significant, since the X chromosome contains a high density of immune-related genes and regulatory elements that are extensively involved in both the innate and adaptive immune responses. Many diseases present with a clear sex bias, and apart from the influence of sex hormones and socioeconomic and behavioural factors, the X chromosome, X-linked genes and X chromosome inactivation mechanisms contribute to this difference. Females are functional mosaics for X-linked genes due to X chromosome inactivation and this, combined with other X chromosome inactivation mechanisms such as genes that escape silencing and skewed inactivation, could contribute to an immunological advantage for females in many infections. In this review, we discuss the involvement of the X chromosome and X inactivation in immunity and address its role in sexual dimorphism of infectious diseases using tuberculosis susceptibility as an example, in which male sex bias is clear, yet not fully explored.
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                Author and article information

                Journal
                Am J Mens Health
                Am J Mens Health
                JMH
                spjmh
                American Journal of Men's Health
                SAGE Publications (Sage CA: Los Angeles, CA )
                1557-9883
                1557-9891
                16 September 2020
                Sep-Oct 2020
                : 14
                : 5
                Affiliations
                [1 ]Roseman University of Health Sciences College of Dental Medicine, South Jordan, UT, USA
                [2 ]Portland State University School of Community Health, Portland, OR, USA
                [3 ]University of Utah School of Medicine, Salt Lake City, UT, USA
                [4 ]Towson University Department of Occupational Therapy & Occupational Science, Towson, MD, USA
                [5 ]George E. Wahlen Department of Veterans Affairs Medical Center, Salt Lake City, UT, USA
                Author notes
                Man Hung, PhD, MED, MSTAT, MSIS, MBA, Research Dean, College of Dental Medicine, Roseman University of Health Sciences, 10894 S. River Front Parkway, South Jordan, UT 84095, USA. Email: mhung@ 123456roseman.edu
                Article
                10.1177_1557988320954021
                10.1177/1557988320954021
                7495118
                32936693
                © The Author(s) 2020

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

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                Review
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                September-October 2020
                ts1

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