Hidden Infections Could Fuel Long Covid, Major Review Suggests
Study: Hidden Infections May Trigger Long Covid Symptoms

A groundbreaking scientific review has proposed a new explanation for the debilitating condition known as long Covid, pointing the finger at hidden, dormant infections that may be reactivated by the initial coronavirus illness.

The Search for a Cause

Affecting an estimated 400 million people globally, long Covid presents a vast array of symptoms from breathlessness and crushing fatigue to cognitive 'brain fog', with no established cure. The fundamental biological cause has remained a stubborn mystery, hampering the development of effective treatments.

Now, a team of 17 leading experts, publishing their analysis in the prestigious journal eLife, argues that the answer may lie not solely with the SARS-CoV-2 virus itself, but with other pathogens it disturbs. "This is an aspect of long Covid that is not talked about a lot," stated microbiologist Dr Maria Laura Gennaro of Rutgers New Jersey Medical School, one of the review's authors.

Dormant Viruses Awakened

The researchers scrutinised existing studies to build their case. A prime suspect is the Epstein-Barr virus (EBV), a common herpesvirus carried latently by about 95% of adults. The review cites one study where two-thirds of long Covid patients showed signs of recent EBV reactivation, with higher antibody levels correlating to more severe symptoms.

"An immune disruption such as Covid can awaken this dormant virus," the review explains, noting that subsequent research has linked EBV reactivation to hallmark long Covid issues like profound fatigue and cognitive difficulties.

Another potential co-conspirator is latent Tuberculosis (TB), carried by a quarter of the world's population. Evidence suggests Covid-19 might deplete the specific immune cells that usually keep TB in check, potentially triggering its reactivation and worsening overall outcomes.

A Path to New Treatments?

The authors outline a biological model where these co-infections could wreak havoc at different stages:

  • If present before Covid, they could leave the immune system compromised from the start.
  • During acute Covid illness, they could compound tissue damage.
  • After the initial infection, they could exploit the lingering immune dysfunction.

This theory opens a tantalising possibility: that existing antibiotics and antivirals could be repurposed to target these underlying infections, offering a new avenue for treatment. However, the scientists are clear that this remains speculative for now.

"Everyone has heard it a million times, but it bears repeating: Correlation doesn't equal causation," cautioned Dr Gennaro. Proving a definitive causal link would require large-scale epidemiological studies and complex animal experiments, the latter hampered by a lack of good animal models for long Covid.

Despite the need for more proof, the central conclusion is clear: effectively treating the millions suffering from long Covid may require looking beyond the coronavirus itself and investigating the hidden microbial landscape it disrupts.