The researchers believe that the "senile" interferon response in older patients leads to severe COVID-19

Researchers in Germany have found that age-dependent damage to the antiviral interferon protein is the basis
for increased susceptibility to severe COVID-19 in older patients.

The immune system's response to SARS-CoV-2 is coordinated by a set of antiviral signaling proteins called interferon, which helps stop viral replication, activates various immune cells, and clears
the virus from the body.

However, whether age-dependent changes in interferon activity explain why older patients are more likely to develop severe COVID-19 is unclear
.

To investigate this problem, a research team led by Dr.

Schnepf explains: "We found that adult animals exhibited rapid, well-coordinated innate and adaptive immune responses to viral infections, while older animals showed reduced, delayed, and more pro-inflammatory responses
.

Schnepf and his colleagues found that the type I interferon signal in the elderly mice was disrupted
.

Schnepf said: "Overall, our data suggest that impaired type I IFN signaling, combined with impaired IFN-γ-mediated immune response, may explain the observed high susceptibility
to SARS-CoV-2 disease in older mice, and possibly in older adults.

Finally, the researchers examined mice that were extremely susceptible to severe COVID-19, that is, older mice that also lacked type I interferon signals
.

Professor Schwemmle said: "By generating and using a mouse model of severe COVID-19, we have identified age-dependent injury to interferon type I and type II responses as a key pathologic mechanism
driving SARS-CoV-2 toxicity in older hosts.

Impaired immune response drives age-dependent severity of COVID-19