It is estimated that 6.5-12.0 % of patients might exhibit persistent symptoms after SARS-CoV-2 infection, including neurological and neurocognitive symptoms. The causes of long COVID (or post-acute sequelae of COVID-19 (PASC)) aren’t fully understood, but research suggests that the persistence of viral material could explain the symptoms. A new study using the golden hamster as a model provides further evidence that SARS-CoV-2 can persist in the brain. The researchers intranasally inoculated male and female hamsters with the ancestral SARS-CoV-2 Wuhan and the Delta and Omicron/BA.1 variants. Although the infected hamsters showed sex and strain differences in clinical signs such as body weight loss during the acute phase of infection, no more clinical sign was detected after 10 days post-infection (dpi). However, at 80 dpi, although considered clinically healthy, the hamsters displayed various neuropsychiatric symptoms and cognitive deficits such as memory impairment. In addition, viral genomic RNA was detected in their brainstem. Transcriptomic analysis of the brainstem also identified persistent alterations in the dopaminergic and glutamatergic signaling as well as in metabolic pathways at 80 dpi, which could potentially cause the neurobehavioral changes.
Original reference: Coleon, A. et al. Nat. commun. 16, 6714 (2025)
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