Why We May Need Viruses More Than Vaccines

Why We May Need Viruses More Than Vaccines

A groundbreaking study published this month in Nature challenges a century old assumption about the innate pathogenicity of these extremely small, self-replicating particles known as viruses. 

Titled, "An enteric virus can replace the beneficial function of commensal bacteria," researchers found that an "enteric RNA virus can replace the beneficial function of commensal bacteria in the intestine." Known as murine (mouse) noravirus (MNV), researchers found that infecting germ-free or antibiotic-treated mice infection with MNV "restored intestinal morphology and lymphocyte function without inducing overt inflammation and disease."

The researchers found:

"Importantly, MNV infection offset the deleterious effect of treatment with antibiotics in models of intestinal injury and pathogenic bacterial infection. These data indicate that eukaryotic viruses have the capacity to support intestinal homeostasis and shape mucosal immunity, similarly to commensal bacteria."

Despite the commonly held belief that viruses are vectors of morbidity and mortality that must be vaccinated against in order to save us from inevitable harm and death, the new study dovetails with a growing body of research showing that our own genome is 8% viral in origin.

Reporting on the new study, in an article well worth reading, the Science Daily states:

"The new findings are the first strong evidence that viruses in the gastrointestinal tract can help maintain health and heal a damaged gut."

They summarized the study's findings as follows:

"The team infected germ-free mice and antibiotic-treated mice with MNV and found that the infection triggered the repair of intestinal tissue damaged by inflammation, restored intestinal cell numbers, restored intestinal cell function, and normalized tissue architecture. The results were apparent after just 2 weeks of MNV infection.

Infection with MNV also helped restore the gut's immune system. The investigators do not yet know how the virus supports the immune system. They did find, however, increased signaling by antiviral type 1 interferon proteins, suggesting the virus was playing a key role in driving the immune response.

The investigators also documented a doubling of T-cell levels in the blood and detectable levels of antibodies in the gut and blood of antibiotic-treated mice after MNV infection. These measures were consistent with a normalization of the immune response. The authors conclude that viral infection of the gut may be helpful once antibiotic treatment has wiped out intestinal bacteria.

Treatment with MNV was also able to improve survival in antibiotic-treated mice receiving the damaging chemical dextran sodium sulphate."

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