When you choose to publish with PLOS, your research makes an impact. Make your work accessible to all, without restrictions, and accelerate scientific discovery with options like preprints and published peer review that make your work more Open.

PLOS BLOGS Speaking of Medicine

PLOS Pathogens’ COVID-19 response

Michael Malim and Kasturi Haldar, Editors-in-Chief of PLOS Pathogens, share the journal’s plan to accelerate and amplify COVID-19 research.

Open and readily available research

This is a time of great challenges and great opportunities for scientists and clinicians working on COVID-19. PLOS Pathogens is committed to building and communicating a robust knowledge base for present and future research that will benefit patients and society.  We publish the latest discoveries in SARS-CoV-2 research, including reports of novel research, in depth Reviews, and shorter Pearls and Opinion pieces. As an Open Access journal, these articles and the underlying data are available to read and cite immediately. This is of paramount importance to ensure these advances can be read and built upon right from the start.

Expert and accelerated editorial oversight

We have entrusted a team of editors who are leading experts in the field, comprised of:

  • Michael Diamond, MD, PhD, Washington University School of Medicine in St. Louis
  • Ron Fouchier, PhD, Erasmus University Medical Center
  • Benhur Lee, MD, Icahn School of Medicine at Mount Sinai
  • Andrew Pekosz, PhD, Johns Hopkins Bloomberg School of Public Health
  • Kanta Subbarao, MBBS, MPH, The Peter Doherty Institute for Infection and Immunity
  • David Wang, PhD, Washington University School of Medicine in St. Louis

This team is committed to accelerating the time to both review and publication. We strive to make an initial editorial decision (reject or review) within three days of editor assignment.

PLOS Pathogens provides a perfect home for your SARS-CoV-2 research

PLOS Pathogens welcomes submissions on the full range of COVID-19 research, including: virology, structural biology, evolution, host interactions, immune responses, pathogenesis, co-morbidities, diagnostics, public health & infection control, vaccines, drug discovery, and clinical trials.

The PLOS-wide COVID-19 collection contains all published COVID-19 research from the full PLOS portfolio. PLOS Pathogens articles will be added to this page upon publication, so papers are accessible across all disciplines.

Learn how to submit.

Mike Diamond
Andy Pekosz
Kanta Subbarao
David Wang
Benhur Lee
Ron Fouchier

Image by Pete Linforth from Pixabay

Discussion
  1. It is my hypothesis that COVID-19 infection and subsequent pathology are caused by low dehydroepiandrosterone (DHEA). Old age and testosterone levels can adversely affect DHEA effects. DHEA naturally declines to low levels in old age; old age intensifies COVID-19. DHEA levels around 1 to 3 are very low; comparable to those of old age. From adrenarche (the age 3 to 6 increase in DHEA) we are primarily DHEA organisms until puberty when testosterone increases. This why children exhibit less COVID-19 but very young are more infected. Testosterone can reduce DHEA effectiveness so COVID-19 is less infective in preadolescence. People who exhibit increased testosterone will be more affected by COVID-19. This is why men are more affected than women and why blacks are more affected than whites. Low DHEA will release cytokines; the cytokine storm of COVID-19. Therefore, agents which reduce testosterone should ameliorate COVID-19; dexamethasone reduces testosterone and telmisartan increases DHEA. Stress (cortisol) is antagonistic to DHEA which could explain part of the ongoing increase in COVID-19 at this time. Testosterone is higher in sunshine and urban groups; lack of social distancing could also explain the current increase. Copyright 2020, James Michael Howard, Fayetteville, Arkansas, U.S.A.

Leave a Reply

Your email address will not be published. Required fields are marked *


Add your ORCID here. (e.g. 0000-0002-7299-680X)

Related Posts
Back to top