Glycoprotein C facilitates the spread of VZV


Varicella-zoster virus (VZV) is a prevalent human pathogen that belongs to the α-herpesvirus family. Clinical and epidemiological evidence shows that primary infection causes chickenpox (varicella), which most commonly affects children, while reactivation results in shingles (zoster), which often occurs in older adults.

It is well established that VZV is transmitted via the respiratory route. Following infection of epithelial cells in the respiratory tract, VZV spreads within the body by hijacking leukocytes (white blood cells) and changing their activity. However, the precise mechanism underlying this process is not fully understood.

Now researchers say that they have made great progress in understanding how VZV spreads after initial infection in the respiratory tract. Led by Hannover Medical School researchers, the study indicates that VZV glycoprotein C (gC) enhances the ability of the virus to recruit and highjack leukocytes, therefore improving the spread of the virus within the host.

Evidence shows some viruses modulate leukocyte migration via the regulation of chemokine activity. Chemokines, a family of signaling proteins, play an essential role in the induction of leukocyte migration. The researchers wondered whether VZV influences the function of chemokines. To address this, they investigated VZV glycoprotein C (gC) because previous studies highlighted a potential role of gC in VZV pathogenesis.

Results showed that recombinant soluble VZV gC ectodomain (rSgC) binds chemokines and enhances chemokine-dependent leukocyte migration. VZV rSgC promotes chemokine activity and therefore promotes the migration of several cell types, including human tonsillar leukocytes. Tonsillar leukocytes are a major target of VZV during primary infection.

The researchers also found that VZV viral particles lacking gC exhibited a reduced ability to enhance chemokine-dependent leukocyte migration. Collectively, the data suggest that VZV gC activity increases the chemokine-mediated attraction of leukocytes to the site of infection and thereby improves the spread of the virus within the host.

The findings were published in the journal PLoS Pathogens on May 25, 2017. More research is required to better elucidate the role of VZV gC activity in virus spread and pathogenesis.
 
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