Ultrastructural Variation of Type II Pneumocytes of BALF of COVID-19 Patients

Type II pneumocytes synthesize alveolar surfactant, which maintains lung airway stability, reduces alveolar surface tension, aids in lung repair, and prevents collapse of alveoli and airway walls. Studies based on immunofluorescence (IF), scanning electron microscopy (SEM), and transmission electron microscopy (TEM) have reported ultrastructural changes and infectivity levels in type II pneumocytes from bronchoalveolar fluid (BALF) of mild-to-severe coronavirus disease 2019 (COVID-19) patients across different age groups (≤60 and ≥60 y) with common comorbidities, such as diabetes, liver and kidney disease, and carcinoma. The localization of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has also been studied using IF and TEM. The BALF samples from the patients without comorbidities showing a high viral load, whereas diabetic patients exhibited the most severe ultrastructural damage among comorbid groups. The overexpression of angiotensin-converting enzyme 2 (ACE2) and TMPRSS2 facilitates SARS-CoV-2 entry and replication in type II pneumocytes, ultimately causing diffuse alveolar damage, increased mucin production, and heightened inflammatory response, leading to respiratory distress and lung dysfunction. This chapter explores the ultrastructural effects of SARS-CoV-2 on type II pneumocytes, analyzing the differences between younger and older patients, both with and without comorbidities. Ultrastructural detailing of viral localization within these cells provides critical insights into disease progression, host vulnerability, and potential therapeutic interventions.