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Why is COVID-19 killing more men than women? WVU immunologist discusses possibilities

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Jennifer Franko, teaching assistant professor, WVU School of Medicine, Department of Microbiology, Immunology and Cell Biology. (WVU Photo)

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Being a man doesn’t make someone more likely to be infected with SARS-CoV-2—the virus that causes COVID-19—but it might make him more likely to have severe complications or die from it. 

According to Jennifer Franko—a teaching assistant professor in the West Virginia University School of Medicine who studies sex differences in immune responses—many factors contribute to sex-linked immunological differences, including variations in sex hormones and genetics. 

Part of the Department of Microbiology, Immunology and Cell Biology, Franko is available to discuss how these immunologic differences might make a virus more dangerous for male patients.


Jen Franko audio file: “I think what ends up happening…”

“In general, men tend to be more susceptible to infection than women. While this difference may or may not be specific to coronaviruses, similar trends were seen in previous coronavirus outbreaks, including Severe Acute Respiratory Syndrome (SARS) in 2003 and Middle East Respiratory Syndrome (MERS) in 2012. In both of these instances, higher mortality rates were reported in males versus females. It’s the same situation that we’re seeing now with SARS-CoV-2.”

“A less robust immune response in males may result in slower viral clearance and poorer outcomes. Such differences in male versus female immune responses may be the result of hormonal or genetic factors. For example, in females, estrogen and progesterone are typically thought to stimulate the immune system and may provide a higher level of protection against infection. In males, testosterone may suppress such a response.”  

“From a genetics standpoint, many immune-related genes are encoded on the X chromosome. Females have two copies of the X chromosome. Males have only one. In order to balance the dosage of X-linked genes between males and females, one female X chromosome is typically inactivated. Interestingly, we are now beginning to realize that not all of those X-chromosome-linked genes are inactive all the time. In some instances, these genes escape inactivation, resulting in a double dosage effect and higher levels of gene expression in females. If these are immune-related genes, they may correlate with stronger immune responses. This may be an additional reason why females respond to infection with more robust responses.”

“Scientists are also interested in determining if the strong male bias is the result of male patients’ possessing more underlying conditions that may amplify their risk—for example, hypertension or heart disease. We also don’t know if differences in ACE-2 receptor expression—the receptor required for viral entry—may contribute to differences in viral load between males and females.” -- Jennifer Franko, teaching assistant professor, WVU School of Medicine, Department of Microbiology, Immunology and Cell Biology

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