Protective Levels of Varicella-Zoster Antibody Did Not Effectively Prevent Chickenpox in an X-Linked Agammaglobulinemia Patient

Nobre, Fernanda Aimée; Gonzalez, Isabela Garrido da Silva; Moraes-Pinto, Maria Isabel de; Costa‐Carvalho, Beatriz Tavares

doi:10.1590/s0036-46652015000500017

Cited by 5 publications

(2 citation statements)

References 17 publications

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“…Finally, chronic fecal shedding of norovirus is very common in XLA children, occurring in 40% of cases (150). Interestingly, EBV and herpes-viral infections are only rarely reported in these patients (112,117,151).…”

Section: Xla and Ar Agammaglobulinemiamentioning

confidence: 99%

Peripheral B Cell Deficiency and Predisposition to Viral Infections: The Paradigm of Immune Deficiencies

et al. 2021

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In the era of COVID-19, understanding how our immune system responds to viral infections is more pertinent than ever. Immunodeficiencies with very low or absent B cells offer a valuable model to study the role of humoral immunity against these types of infection. This review looks at the available evidence on viral infections in patients with B cell alymphocytosis, in particular those with X-linked agammaglobulinemia (XLA), Good’s syndrome, post monoclonal-antibody therapy and certain patients with Common Variable Immune Deficiency (CVID). Viral infections are not as infrequent as previously thought in these conditions and individuals with very low circulating B cells seem to be predisposed to an adverse outcome. Particularly in the case of SARS-CoV2 infection, mounting evidence suggests that peripheral B cell alymphocytosis is linked to a poor prognosis.

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Section: Xla and Ar Agammaglobulinemiamentioning

confidence: 99%

Peripheral B Cell Deficiency and Predisposition to Viral Infections: The Paradigm of Immune Deficiencies

et al. 2021

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“…The biological importance of VZV-specific antibodies in vivo is unclear. Although patients with agammaglobulinemia are not more susceptible to severe varicella infection (62), treatment of some immunocompromised children and pregnant women with VariZIG (high-titer VZV polyclonal sera) has been shown to prevent severe varicella (17)(18)(19)(20). Additionally, VZV-specific total antibody titers do not decrease with age (9).…”

Section: Figmentioning

confidence: 99%

Breadth and Functionality of Varicella-Zoster Virus Glycoprotein-Specific Antibodies Identified after Zostavax Vaccination in Humans

Sullivan

Reuter-Monslow

Sei

et al. 2018

J Virol

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Herpes zoster (HZ) (shingles) is the clinical manifestation of varicella-zoster virus (VZV) reactivation. HZ typically develops as people age, due to decreased cell-mediated immunity. However, the importance of antibodies for immunity against HZ prevention remains to be understood. The goal of this study was to examine the breadth and functionality of VZV-specific antibodies after vaccination with a live attenuated HZ vaccine (Zostavax). Direct enumeration of VZV-specific antibody-secreting cells (ASCs) via enzyme-linked immunosorbent spot assay (ELISPOT assay) showed that Zostavax can induce both IgG and IgA ASCs 7 days after vaccination but not IgM ASCs. The VZV-specific ASCs range from 33 to 55% of the total IgG ASCs. Twenty-five human VZV-specific monoclonal antibodies (MAbs) were cloned and characterized from single-cell-sorted ASCs of five subjects (>60 years old) who received Zostavax. These MAbs had an average of ∼20 somatic hypermutations per VH gene, similar to those seen after seasonal influenza vaccination. Fifteen of the 25 MAbs were gE specific, whereas the remaining MAbs were gB, gH, or gI specific. The most potent neutralizing antibodies were gH specific and were also able to inhibit cell-to-cell spread of the virus Most gE-specific MAbs were able to neutralize VZV, but they required the presence of complement and were unable to block cell-to-cell spread. These data indicate that Zostavax induces a memory B cell recall response characterized by anti-gE> anti-gI > anti-gB > anti-gH antibodies. While antibodies to gH could be involved in limiting the spread of VZV upon reactivation, the contribution of anti-gE antibodies toward protective immunity after Zostavax needs further evaluation. Varicella-zoster virus (VZV) is the causative agent of chickenpox and shingles. Following infection with VZV, the virus becomes latent and resides in nerve cells. Age-related declines in immunity/immunosuppression can result in reactivation of this latent virus, causing shingles. It has been shown that waning T cell immunity correlates with an increased incidence of VZV reactivation. Interestingly, serum with high levels of VZV-specific antibodies (VariZIG; IV immunoglobulin) has been administered to high-risk populations, e.g., immunocompromised children, newborns, and pregnant women, after exposure to VZV and has shown some protection against chickenpox. However, the relative contribution of antibodies against individual surface glycoproteins toward protection from shingles in elderly/immunocompromised individuals has not been established. Here, we examined the breadth and functionality of VZV-specific antibodies after vaccination with the live attenuated VZV vaccine Zostavax in humans. This study will add to our understanding of the role of antibodies in protection against shingles.

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Low Rates of Poliovirus Antibodies in Primary Immunodeficiency Patients on Regular Intravenous Immunoglobulin Treatment

et al. 2018

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Protective Levels of Varicella-Zoster Antibody Did Not Effectively Prevent Chickenpox in an X-Linked Agammaglobulinemia Patient

Cited by 5 publications

References 17 publications

Peripheral B Cell Deficiency and Predisposition to Viral Infections: The Paradigm of Immune Deficiencies

Peripheral B Cell Deficiency and Predisposition to Viral Infections: The Paradigm of Immune Deficiencies

Breadth and Functionality of Varicella-Zoster Virus Glycoprotein-Specific Antibodies Identified after Zostavax Vaccination in Humans

Low Rates of Poliovirus Antibodies in Primary Immunodeficiency Patients on Regular Intravenous Immunoglobulin Treatment

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