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Chronic varicella zoster, natural killer cells
Chronic varicella zoster virus (VZV) infection is characterized by the persistence of viral DNA in latently infected neurons and the periodic reactivation of the virus, leading to herpes zoster (shingles). Natural killer (NK) cells play a crucial role in the immune response to VZV infection, both during primary infection and latency.
NK Cell Phenotype and Function
Studies have shown that NK cells exhibit altered phenotypes during chronic VZV infection. For example, invariant NK T cells (iNKT) have been found to have low numbers and an altered phenotype in recurrent VZV infection (Novakova et al., 2011). Additionally, VZV has been shown to productively infect human NK cells and manipulate their phenotype (Campbell et al., 2018).
NK Cell Cytotoxicity and Granzyme B
Granzyme B, a key mediator of NK cell cytotoxicity, has been found to cleave multiple VZV gene products, including ORF4, which inhibits NK cell cytotoxicity (Gerada et al., 2019). This suggests that VZV has evolved mechanisms to evade NK cell-mediated immune surveillance.
Implications for Chronic VZV Infection
The altered NK cell phenotype and function during chronic VZV infection may contribute to the persistence of the virus and the development of herpes zoster. Furthermore, the ability of VZV to infect and manipulate NK cells may allow the virus to evade immune detection and persist in a latent state.
Summary
In summary, chronic varicella zoster virus infection is associated with altered natural killer cell phenotypes and functions, including reduced numbers and altered surface markers, as well as productive infection and manipulation of NK cells by the virus. These findings highlight the complex interplay between VZV and the immune system during chronic infection and suggest that NK cells play a critical role in the immune response to VZV.
Chronic varicella zoster virus (VZV) infection is characterized by the persistence of viral DNA in latently infected neurons and the periodic reactivation of the virus, leading to herpes zoster (shingles). Natural killer (NK) cells play a crucial role in the immune response to VZV infection, both during primary infection and latency.
NK Cell Phenotype and Function
Studies have shown that NK cells exhibit altered phenotypes during chronic VZV infection. For example, invariant NK T cells (iNKT) have been found to have low numbers and an altered phenotype in recurrent VZV infection (Novakova et al., 2011). Additionally, VZV has been shown to productively infect human NK cells and manipulate their phenotype (Campbell et al., 2018).
NK Cell Cytotoxicity and Granzyme B
Granzyme B, a key mediator of NK cell cytotoxicity, has been found to cleave multiple VZV gene products, including ORF4, which inhibits NK cell cytotoxicity (Gerada et al., 2019). This suggests that VZV has evolved mechanisms to evade NK cell-mediated immune surveillance.
Implications for Chronic VZV Infection
The altered NK cell phenotype and function during chronic VZV infection may contribute to the persistence of the virus and the development of herpes zoster. Furthermore, the ability of VZV to infect and manipulate NK cells may allow the virus to evade immune detection and persist in a latent state.
Summary
In summary, chronic varicella zoster virus infection is associated with altered natural killer cell phenotypes and functions, including reduced numbers and altered surface markers, as well as productive infection and manipulation of NK cells by the virus. These findings highlight the complex interplay between VZV and the immune system during chronic infection and suggest that NK cells play a critical role in the immune response to VZV.