Respiratory Diseases Roundup

SARS-CoV-2 and RSV Cardiopulmonary Risk Updates

Edited by:
Kate Young

Key Highlights

  • In a mouse model, sublethal SARS-CoV-2 and influenza A both produced persistent lung inflammation and fibrosis, but SARS-CoV-2 was associated with sustained neuroinflammation and hypothalamic-pituitary axis disruption.1
  • Prior SARS-CoV-2 infection was associated with faster progression of coronary plaque, more high-risk plaque features, and higher target lesion failure risk on coronary CT angiography.2
  • In a systematic review and meta-analysis, about 1 in 5 hospitalized adults with RSV disease experienced a cardiac event; heart failure was more frequent after RSV than after influenza.3

Distinct postviral sequelae in mice1

In a recent study, investigators longitudinally evaluated C57BL/6 mice after sublethal infection with mouse-adapted SARS-CoV-2 (MA30) or influenza A (PR8) to characterize subchronic lung and brain effects. Lung and brain tissues were assessed at 14, 21, and 28 days after infection using histologic analysis and bulk RNA sequencing. Both viral infections caused prolonged pulmonary inflammation and fibrosis. However, the pulmonary transcriptional patterns diverged: MA30-infected lungs showed persistent upregulation of inflammatory, coagulation, complement, fibrotic, and extracellular matrix remodeling pathways, whereas PR8-infected lungs showed a stronger acute interferon response and chronic upregulation of basal epithelial markers consistent with epithelial regeneration.

Important differences also emerged in the central nervous system. Neither group had detectable brain infection, but MA30-infected mice had more early microhemorrhages and persistent neuroinflammation across time points, while PR8-infected mice did not. In MA30-infected brains, transcriptomic profiling showed upregulation of extracellular matrix remodeling, vascular dysfunction, IL-6 signaling, and hormone-related pathways, along with suppression of key neurotransmitter-related genes, findings the authors described as consistent with ongoing neurobiological disruption. By contrast, PR8-related brain changes were more limited. The investigators concluded that although both viruses produced sustained lung abnormalities, SARS-CoV-2 induced broader and more persistent brain-related changes in this model.

Prior SARS-CoV-2 infection linked to plaque progression2

A retrospective study evaluated whether prior SARS-CoV-2 infection was associated with coronary inflammation, plaque progression, and adverse cardiovascular outcomes on coronary CT angiography. The analysis included 803 patients and 2588 coronary lesions, including 2108 lesions in patients with prior SARS-CoV-2 infection and 480 lesions in patients without infection. Compared with lesions in patients without prior infection, lesions in patients with SARS-CoV-2 infection showed faster progression of total percent atheroma volume, at 0.90% per year vs 0.62% per year, and noncalcified percent atheroma volume, at 0.78% per year vs 0.42% per year; both differences were statistically significant.

At follow-up, lesions in the SARS-CoV-2 group were also more likely to become high-risk plaques, 21.0% vs 15.8%, and more likely to show elevated pericoronary adipose tissue attenuation, a marker of coronary inflammation, 27.1% vs 19.8%. Target lesion failure occurred more often in lesions from patients with prior SARS-CoV-2 infection, 10.4% vs 3.1%, with an adjusted hazard ratio of about 2.9. The report further noted that coronary inflammation partially mediated the association between SARS-CoV-2 infection and plaque progression. Overall, the findings suggest that prior SARS-CoV-2 infection was associated with accelerated progression of higher-risk coronary plaque features and worse lesion-level cardiovascular outcomes.

RSV disease carries cardiac event risk3

A systematic literature review and meta-analysis assessed the absolute and relative risk of cardiac events after respiratory syncytial virus (RSV) disease in adults. Investigators searched Embase, PubMed, and gray literature sources for studies published from January 1, 2000, through March 6, 2024, and included 28 studies out of 3887 screened publications. Most data came from hospitalized populations. Across 25 studies of hospitalized patients with RSV disease, the pooled estimate for any cardiac event was 19.2% (95% CI, 15.1%-24.2%). Pooled estimates were 15.7% (95% CI, 14.8%-16.5%) for heart failure and 5.4% (95% CI, 3.1%-9.5%) for acute coronary syndrome. Cardiac event-related mortality ranged from 1.1% to 9.8%.

When outcomes were compared with influenza, RSV disease was associated with a higher risk of any cardiac event, with a risk ratio of 1.2 (95% CI, 1.1-1.4), and a higher risk of heart failure, with a risk ratio of 1.3 (95% CI, 1.1-1.6). The risk ratio for acute coronary syndrome was 1.2 (95% CI, 0.9-1.5), suggesting less certainty for that endpoint. The authors concluded that RSV in adults, particularly among older hospitalized patients, carries clinically meaningful cardiovascular risk beyond respiratory illness alone and said more work is needed to define the timing and duration of post-RSV cardiac risk more precisely.

References

  1. Currey J, Wang C, Mayer MG, et al. Characterization of subchronic lung and brain consequences caused by mouse-adapted SARS-CoV-2 and influenza A infection of C57BL6 mice. Front Immunol. 2026;17:1755141. Published 2026 Feb 25. doi:10.3389/fimmu.2026.1755141
  2. Dai N, Tang X, Hu Y, et al. SARS-CoV-2 Infection Association with Atherosclerotic Plaque Progression at Coronary CT Angiography and Adverse Cardiovascular Events. Radiology. 2025;314(2):e240876. doi:10.1148/radiol.240876
  3. Montiel J, Williams E, Robles-Rodríguez WG, et al. The risk of cardiac disease events after respiratory syncytial virus disease: a systematic literature review and meta-analysis. Eur Respir Rev. 2026;35(179):250160. Published 2026 Jan 28. doi:10.1183/16000617.0160-2025