New research conducted by the Institut Pasteur and the French public research institute CEA has revealed that the SARS-CoV-2 virus can persist in the lungs of recovered individuals for up to 18 months after infection. This challenges the previous belief that recovery from COVID-19 meant the complete eradication of the virus from the body. The study, which focused on lung cells in a preclinical model of non-human primates, found that the virus was still present in the lungs of certain individuals for an extended period, even when it was undetectable in the upper respiratory tract. The findings shed light on the complexities of the human immune response to SARS-CoV-2.
One of the key findings of the study was the discovery of viral reservoirs in the lungs. These reservoirs are locations where the virus can persist after an initial infection. In the case of SARS-CoV-2, the researchers found that the virus could remain in certain immune cells, specifically alveolar macrophages, within the lungs. Even when conventional tests showed no trace of the virus in the upper respiratory tract or blood, the virus was still found in these immune cells. This discovery challenges the assumption that the absence of detectable virus in the upper respiratory tract indicates the complete elimination of the virus from the body.
The study also investigated the role of innate immunity, the body’s first line of defense against pathogens, in the persistence of SARS-CoV-2. Natural killer (NK) cells, a crucial component of innate immunity, were found to play a significant role in controlling viral infections. In some individuals, infected macrophages in the lungs became resistant to destruction by NK cells, allowing the virus to persist. However, in other individuals, adaptive NK cells were able to adapt to the infection and destroy the infected cells. This variability in the effectiveness of innate immunity suggests a potential connection to the phenomenon of long COVID, where individuals experience prolonged symptoms after recovering from the acute phase of the disease.
The study also delved into the molecular mechanisms involved in the persistence of SARS-CoV-2 in the lungs. It was found that interferon-gamma (IFN-γ), a cytokine involved in antiviral responses, played a crucial role in controlling viral replication in alveolar macrophages. However, impaired IFN-γ production was observed in some individuals, which allowed the virus to replicate and persist in these cells. This highlights the complexity of the immune response to SARS-CoV-2 and the role of cytokines in controlling viral persistence.
The research was conducted using non-human primate models, specifically cynomolgus macaques, which provided valuable insights into immune cell functioning and responses in tissues. The study used comprehensive techniques to analyze lung cells and revealed alterations in macrophage phenotype and lymphocyte frequencies in infected macaques. This information contributes to our understanding of SARS-CoV-2 persistence and the immune response.
Overall, this study offers important insights into the persistence of SARS-CoV-2 in the lungs and the complexity of the immune response to the virus. The findings have implications for understanding the long-term consequences of COVID-19 and developing targeted therapeutic interventions. As further research is conducted, it is hoped that a deeper understanding of viral persistence will be gained, shedding light on the mysteries of long COVID.