# Histopathological and Immunohistochemical Findings in Postmortem Lungs from Mexican Patients with Severe COVID-19

**Authors:** Laura Guadalupe Chávez Gómez, Diana Gabriela Ríos Valencia, Tania Lucía Madrigal-Valencia, Lilian Hernández Mendoza, Armando Pérez-Torres, Rocio Tirado Mendoza

PMC · DOI: 10.3390/ijms27021049 · 2026-01-21

## TL;DR

This study examines lung tissue from Mexican patients who died of severe COVID-19 to identify histopathological and immunohistochemical changes caused by the virus.

## Contribution

The study provides new insights into the lung pathology of severe COVID-19 in Mexican patients using postmortem samples and immunohistochemistry.

## Key findings

- All nine samples showed diffuse alveolar damage, with some showing no alveolar space and pleural fibrosis.
- Immunohistochemistry revealed Spike-positive inclusion bodies in type I pneumocytes in several samples.
- H&E staining showed eosinophilic inclusion bodies and vascular congestion, suggesting tissue damage linked to severe symptoms.

## Abstract

During the COVID-19 pandemic, SARS-CoV-2 quickly spread all over the world in a pattern of waves. In Mexico, the first wave was from March 2020 to September 2020, and during this time autopsies were forbidden. After that, the postmortem lung samples allowed us to identify histological alterations because of COVID-19. Moreover, SARS-CoV-2 infections are characterized by the manifestation of cytopathic effects like inclusion bodies, and multinucleated cells in alveolar spaces and alveolar walls. Additionally, atypical, enlarged cells, presence of macrophages in alveolar spaces, and congestion of vascular vessels were the other histopathologic alterations of the lung. Our study covered the analysis of nine postmortem lung samples from patients with severe COVID-19 diagnosed by qRT-PCR. The samples were stained with Hematoxylin-Eosin to identify the histological alterations related to lung architecture and cell populations and were subjected to immunohistochemistry for the SARS-CoV-2 Spike and Nucleocapsid proteins. All samples showed alterations associated with diffuse alveolar damage and 1/9 presented no alveolar space, 5/9 presented different levels of pleural fibrosis, and 4/9 presented distention of the small capillaries. Immunohistochemistry results revealed that 4/9 samples showed Spike-positive cytoplasmic inclusion bodies in type I pneumocytes and 2/9 Spike-positive nuclear inclusion bodies in type I pneumocytes. These inclusion bodies were found to be eosinophilic with H&E stains. The H&E results suggest tissue alterations that may contribute to the signs and symptoms of severe COVID-19, as well as the Spike protein expression, as its distribution suggests its participation in pathophysiology.

## Linked entities

- **Diseases:** COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** S (surface glycoprotein) [NCBI Gene 43740568] {aka spike glycoprotein}
- **Diseases:** COVID-19 (MESH:D000086382), infections (MESH:D007239), pleural fibrosis (MESH:D005355)
- **Chemicals:** H&amp;E (MESH:D006371), Hematoxylin (MESH:D006416)
- **Species:** Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606]

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12841879/full.md

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Source: https://tomesphere.com/paper/PMC12841879