Evidence map›Paper›PMID 33063089›Full record

ReviewCardiovascular research2020

Higher mortality of COVID-19 in males: sex differences in immune response and cardiovascular comorbidities.

Laura A Bienvenu, Jonathan Noonan, Xiaowei Wang, Karlheinz Peter

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
179citing papers in PubMed, 3 pooled it
7.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

179 citing papers in PubMed, 3 syntheses or guidelines pooled it, 357 citations in OpenAlex.

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119 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 2 countries.

Laura A BienvenuAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC 3004, Australia.
Jonathan NoonanAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC 3004, Australia.
Xiaowei WangAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC 3004, Australia.
Karlheinz PeterAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, VIC 3004, Australia.
Baker Heart and Diabetes Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The high mortality rate of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection is a critical concern of the coronavirus disease 2019 (COVID-19) pandemic. Strikingly, men account for the majority of COVID-19 deaths, with current figures ranging from 59% to 75% of total mortality. However, despite clear implications in relation to COVID-19 mortality, most research has not considered sex as a critical factor in data analysis. Here, we highlight fundamental biological differences that exist between males and females, and how these may make significant contributions to the male-biased COVID-19 mortality. We present preclinical evidence identifying the influence of biological sex on the expression and regulation of angiotensin-converting enzyme 2 (ACE2), which is the main receptor used by SARS-CoV-2 to enter cells. However, we note that there is a lack of reports showing that sexual dimorphism of ACE2 expression exists and is of functional relevance in humans. In contrast, there is strong evidence, especially in the context of viral infections, that sexual dimorphism plays a central role in the genetic and hormonal regulation of immune responses, both of the innate and the adaptive immune system. We review evidence supporting that ineffective anti-SARS-CoV-2 responses, coupled with a predisposition for inappropriate hyperinflammatory responses, could provide a biological explanation for the male bias in COVID-19 mortality. A prominent finding in COVID-19 is the increased risk of death with pre-existing cardiovascular comorbidities, such as hypertension, obesity, and age. We contextualize how important features of sexual dimorphism and inflammation in COVID-19 may exhibit a reciprocal relationship with comorbidities, and explain their increased mortality risk. Ultimately, we demonstrate that biological sex is a fundamental variable of critical relevance to our mechanistic understanding of SARS-CoV-2 infection and the pursuit of effective COVID-19 preventative and therapeutic strategies.

Indexed as

Health Status DisparitiesAnimalsCardiovascular DiseasesComorbidityCOVID-19FemaleHost-Pathogen InteractionsHumansInflammationMalePrognosisRisk AssessmentRisk FactorsSARS-CoV-2Sex CharacteristicsSex FactorsCardiovascular comorbiditiesCOVID-19InflammationSARS-CoV-2Sex differences

Identifiers

PMID33063089
PMCPMC7665363
OpenAlexW3093131949

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.