Autoantibodies in Shingles Virus May Drive Postherpetic Neuralgia

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Autoantibodies in Shingles Virus May Drive Postherpetic Neuralgia
Autoantibodies in Shingles Virus May Drive Postherpetic Neuralgia

Some patients who develop painful postherpetic neuralgia (PHN) following varicella zoster virus (VZV) reactivation may have several sporadic anti-cytokine autoantibodies present, creating a deficit in immune signaling.

The immunodeficiency syndrome in these patients may increase susceptibility to PHN, according to findings by Ahmad Bayat, MD, of the National Institutes of Health, and colleagues.

The study, published in the Journal of Translational Medicine, documents the presence of autoantibodies against several cytokines and other autoantigens in patients with herpes zoster (HZ) who have or don't have PHN.

Dr. Bayat and colleagues collected sera samples from 115 HZ patients with PHN and 83 without PHN. A cohort of patients with complex regional pain syndrome or neuropathic pain was also tested against the selected cytokines as controls. Antibody levels against VZV, Epstein Barr virus, and herpes simplex virus-2 were also tested in patients with HZ and PHN.

CLINICAL CHART: Neuropathic Pain Treatments

Six patients with PHN showed markedly elevated levels of single, autoantibodies against interferon-α, interferon-γ, GM-CSF, or interleukin-6, while those with HZ without PHN and the pain control group showed low or no autoantibodies against the four cytokines. One PHN patient with high levels of anti-interleukin-6 autoantibodies had a significantly depressed antibody level to VZV, which possibly reflects poor T-cell immunity against VZV. Further, in vitro functional testing showed that 3 of the 5 PHN patients who tested positive for anti-cytokine autoantibody had neutralizing autoantibodies against interferon-α, GM-CSF, or interleukin-6, compared to none of the HZ patients without PHN. This finding suggests that anti-cytokine immunodeficiency may contribute to development of PHN.

“It is likely that the development of PHN is a highly complex, multifactorial process driven by many subtle genetic, environmental, and acquired factors,” the authors wrote. “Since autoantibodies and decline in immune system function are known to occur more commonly in older subjects the present observations suggest the likelihood that there may be additional, unrecognized pathogenic autoantibodies against other immune components in older subjects that may increase susceptibility to PHN.”


  1. Bayat A et al. J Transl Med. 2015; doi:10.1186/s12967-015-0695-6.
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