COPD and Herpes Zoster: Risk and Immunization
Sneha ShresthaAbhigan Babu ShresthaAbhyuday YadavSuyesh Raj ShresthaSelene PokharelSajina ShresthaLok Kumar Shrestha
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Abstract:
Varicella Zoster is a neurotropic virus which leads to acute varicella or it may lay dormant in the spinal root ganglion. Reactivation of varicella zoster causes Herpes Zoster (HZ) and occurs commonly in immunosuppressed conditions like COPD. Severity of Herpes Zoster is also higher among those with comorbidities like COPD. Even among COPD patients, the severity of HZ is said to be higher among those using oral corticosteroids than those using inhaled steroids due to greater immunosuppressive effect. It has also been found that incidence rate of COPD exacerbations, transient ischemic attack and stroke are higher among COPD patients with HZ compared to those without HZ. Herpes zoster vaccinations prevent reactivation of latent HZ and reduce the associated complications. Live attenuated and recombinant vaccines are available for vaccination among which recombinant vaccine is found to be more effective. The cost burden due to HZ among COPD patients was also higher compared to those without HZ. Childhood varicella vaccination is cost effective, however cost effectiveness of adolescent vaccination is unclear.Keywords:
Varicella zoster virus
Journal Article Age-Related Differences In Cell-Mediated Immunity To Varicella-Zoster Virus Among Children And Adults Immunized With Live Attenuated Varicella Vaccine Get access Sonia Nader, Sonia Nader Department of Pediatrics, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California Search for other works by this author on: Oxford Academic PubMed Google Scholar Randy Bergen, Randy Bergen Department of Pediatrics, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California Search for other works by this author on: Oxford Academic PubMed Google Scholar Margaret Sharp, Margaret Sharp Department of Pediatrics, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California Search for other works by this author on: Oxford Academic PubMed Google Scholar Ann M. Arvin Ann M. Arvin Department of Pediatrics, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, California Reprints or correspondence: Dr. Ann M. Arvin, Dept. of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305. Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 171, Issue 1, January 1995, Pages 13–17, https://doi.org/10.1093/infdis/171.1.13 Published: 01 January 1995 Article history Received: 13 May 1994 Revision received: 25 August 1994 Published: 01 January 1995
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We present the case of a 4-year-old immunocompetent girl with varicella-zoster virus (VZV) that occurred 45 months after a single dose of the varicella vaccine. Varicella-zoster virus is rare in children, particularly those who have received the varicella vaccine. Our case illustrates the need for a continued high index of suspicion, even among vaccinated children with herpetiform rashes, for varicella reactivation or reinfection.
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SUMMARY The licensure and recommendation of varicella vaccine in the mid-1990s in the United States have led to dramatic declines in varicella incidence and varicella-related deaths and hospitalizations. Varicella outbreaks remain common and occur increasingly in highly vaccinated populations. Breakthrough varicella in vaccinated individuals is characteristically mild, typically with fewer lesions that frequently do not progress to a vesicular stage. As such, the laboratory diagnosis of varicella has grown increasingly important, particularly in outbreak settings. In this review the impact of varicella vaccine on varicella-zoster virus (VZV) disease, arising complications in the effective diagnosis and monitoring of VZV transmission, and the relative strengths and limitations of currently available laboratory diagnostic techniques are all addressed. Since disease symptoms often resolve in outbreak settings before suitable test specimens can be obtained, the need to develop new diagnostic approaches that rely on alternative patient samples is also discussed.
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(See the article by Nagel et al, on pages 820–4.)
The development and deployment of varicella vaccine in the United States has almost eliminated chickenpox [1], but herpes zoster (HZ), which is due to reactivation of latent varicella-zoster virus (VZV), remains very much with us [2]. Since 2006, the live attenuated zoster vaccine, similar to but 14 times stronger than varicella vaccine, has been used to prevent HZ by boosting cellular immunity to VZV in older individuals [3]. The zoster vaccine, however, has not achieved widespread uptake for complex reasons, including problematic availability and high expense [4]. Simultaneously with VZV vaccination programs, molecular virologic techniques have emerged and have proven extremely useful, in particular polymerase chain reaction (PCR), for diagnosis of diseases caused by VZV [5–7]. These diseases include cases of mild varicella, HZ, cranial nerve palsies, VZV encephalitis/meningitis, various ocular diseases, and zoster without rash (zoster sine herpete). PCR may be used not only to diagnose these diseases but also to determine if the VZV in question is the wild type or the Oka vaccine strain [8]. PCR for VZV is mostly performed on specimens from skin rashes or cerebrospinal fluid, but recently PCR has been used to diagnose varicella and HZ using saliva.
What is the history of examining saliva for diagnosis of herpesvirus infections? Around the beginning of this century, a transient decrease in normal immune function was demonstrated by scientists at NASA in astronauts following space travel, which was ascribed to stress responses (eg, increased blood cortisol levels) experienced during space flight [9]. Asymptomatic reactivation of Epstein-Barr virus [10, 11] and cytomegalovirus [9] was demonstrated in astronauts, in some instances by examining saliva for viral DNA. Mehta and colleagues then found VZV DNA in saliva in 30% of asymptomatic astronauts, both during and after space flights [12]. This impressive observation led to a study of whether VZV DNA was present in saliva of patients with clinical HZ. In a critical diagnostic study on elderly individuals who were not astronauts, salivary VZV DNA was demonstrated in 54 of 54 patients with HZ [6].
In a follow-up study from the Gilden laboratory, included in this issue of the Journal, an effort was made to determine if postherpetic neuralgia (PHN) complicating and following HZ might be associated with the prolonged presence of VZV DNA in saliva, suggesting chronic ganglionic infection [13]. The saliva of elderly patients with and without a history of PHN after HZ, as well as healthy elderly controls with no history of HZ, was tested for VZV DNA. Among HZ patients, 21 of 32 (67%) had VZV DNA in saliva, compared with 2 of 17 (12%) controls (P = .001). Perhaps unexpectedly, however, the presence of salivary VZV DNA was similar in patients following HZ, whether they had PHN or not. This suggested that prolonged replication of VZV is unlikely to explain PHN, which has therapeutic implications regarding prolonged antiviral therapy for this often-severe illness. Interestingly, this result was not exactly in agreement with the hypotheses of these investigators; earlier studies had suggested prolonged VZV replication in patients with PHN. On the other hand, the current results provide a clue as to how VZV might stimulate long-term immunity to the virus, by subclinical reactivation with resultant stimulation of specific immune responses.
Like many successful research investigations, the current study raises a number of additional questions. One is why is VZV DNA present in saliva? This finding is understandable if a zoster rash is on or near the face, but even people with a zoster rash on the extremities have VZV DNA in saliva. Does this indicate that reactivation of VZV occurs in distant dermatomes at the same time? If so, why should VZV frequently reactivate simultaneously in the trigeminal ganglion and in a distant ganglion? Might such a phenomenon be related to the VZV latency burden in ganglia in various locations? Is asymptomatic reactivation of VZV common, and does it produce VZV in saliva? It would be useful to have additional information on larger numbers of healthy individuals, further refining what percentage of varicella-immune individuals shed VZV DNA in saliva over time. Finally, because VZV DNA is present in saliva after vaccination to prevent HZ [14], is this the result of viremia that leads to VZV DNA in saliva, and how is this mechanism related to what occurs in HZ?
There has been great interest in an illness that has been termed zoster sine herpete, or HZ without rash, for many years. Clinicians are used to rejecting VZV from the differential diagnosis in patients if no rash is present even though the patient may have other symptoms of VZV infection such as unexplained unilateral pain or cranial nerve paralysis. It is becoming clear, thanks in great part to the use of PCR, that VZV can cause disease without rash. Possibly the first recognition of this phenomenon was in patients infected with human immunodeficiency virus who developed VZV encephalitis without rash [15–17]. In these patients, the diagnosis was made by detecting VZV DNA in cerebrospinal fluid. It was then observed that in significant numbers of patients with facial paralysis without rash, VZV DNA was also demonstrable in their saliva [18]. Now one wonders whether individuals who have dermatomal pain in the absence of facial paralysis and rash, true zoster sine herpete, also may have HZ that can be demonstrated by studying their saliva.
Recently, it has been found that VZV DNA is frequently present in saliva and urine in patients with varicella [5]. Interestingly, the time-honored means of identifying VZV disease, measuring antibodies in acute and convalescent serum samples, does not seem to measure up to PCR in either sensitivity or rapidity, and may be simply outdated for diagnosis of disease [5].
Another question remains regarding detection of salivary VZV DNA for diagnosis. What is the best method to collect saliva? A variety of collectors are commercially available, and some investigators have simply used swabs for this purpose. The most sensitive and specific means to identify VZV DNA in saliva deserves further exploration. In addition, more information on the possible infectiousness of VZV in saliva is necessary and could have utility for infection control.
At present, however, it is clear that identifying VZV in saliva is becoming a useful, rapid, and noninvasive means for diagnosis of VZV infection. Although it does not seem that there is a causal relationship of the presence of VZV DNA and PHN, the persistence of the viral footprint after clinical disease deserves further exploration to uncover its true meaning.
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Background. Varicella-zoster virus (VZV)-specific cell-mediated immunity is important for protection against VZV disease. We studied the relationship between VZV cell-mediated immunity and age after varicella or VZV vaccination in healthy and human immunodeficiency virus (HIV)-infected individuals. Methods. VZV responder cell frequency (RCF) determinations from 752 healthy and 200 HIV-infected subjects were used to identify group-specific regression curves on age. Results. In healthy individuals with past varicella, VZV RCF peaked at 34 years of age. Similarly, VZV-RCF after varicella vaccine increased with age in subjects aged <1 to 43 years. In subjects aged 61–90 years, VZV RCF after zoster vaccine decreased with age. HIV-infected children had lower VZV RCF estimates than HIV-infected adults. In both groups, VZV RCF results were low and constant over age. Varicella vaccination of HIV-infected children with CD4 levels ⩾20% generated VZV RCF values higher than wild-type infection and comparable to vaccine-induced responses of healthy children. Conclusions. In immunocompetent individuals with prior varicella, VZV RCF peaked in early adulthood. Administration of varicella vaccine to HIV-infected or uninfected individuals aged >5 years generated VZV RCF values similar to those of immunocompetent individuals with immunity induced by wild-type infection. A zoster vaccine increased the VZV RCF of elderly adults aged <75 years to values higher than peak values induced by wild-type infection.
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Herpes zoster, may be severe and recurrent in HIV-infected children. We determined the safety and immunogenicity of live attenuated varicella-zoster virus (VZV) vaccine in 46 HIV-infected children who had experienced varicella. There were no serious adverse events. Two years after vaccination 82% of subjects remained VZV-antibody positive and 60% had VZV-specific cell-mediated immunity. No child developed herpes zoster.
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OBJECTIVE: To review the varicella-zoster virus (VZV) and herpes zoster disease and to summarize published reports on the use of the live-attenuated varicella zoster vaccine to enhance cell-mediated immunity in elderly individuals. DATA SOURCE: A MEDLINE search (1966–August 1999) for English-language clinical studies and review articles pertaining to VZV and the live-attenuated varicella vaccine was conducted; references obtained from these publications were subsequently reviewed for additional relevant articles. STUDY SELECTION AND DATA EXTRACTION: Representative clinical trials were summarized and relevant information was selected to assist in the understanding of VZV, the subsequent immune response, and the live-attenuated varicella vaccine. DATA SYNTHESIS: The physiologic, age-related decline in VZV cell–mediated immunity has been shown to be restored on administration of live-attenuated varicella vaccine. Various studies report serum anti-VZV antibody concentrations, and production of interferon-gamma were increased following vaccination. Concentrations subsequently returned to baseline one year after vaccination. Increase in responder cell frequency, a measure of cell-mediated immunity, has been reported to last up to four years after vaccination, at concentrations similar or superior to those observed following herpes zoster. CONCLUSIONS: Enhancement of cell-mediated immune response in elderly individuals through vaccination with live-attenuated varicella vaccine is a possible measure to protect this population from herpes zoster and to attenuate its complications. A summary of immunogenicity studies to identify the immune response to live-attenuated varicella vaccine in the elderly is presented. The absolute clinical significance, as well as appropriate administration guidelines of this prophylactic intervention, will become evident following forthcoming large, masked, placebo-controlled trials.
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OBJECTIVE:To review the varicella-zoster virus (VZV) and herpes zoster disease and to summarize published reports on the use of the live-attenuated varicella zoster vaccine to enhance cell-mediated immunity in elderly individuals.DATA SOURCE:A MEDLINE search (1966–August 1999) for English-language clinical studies and review articles pertaining to VZV and the live-attenuated varicella vaccine was conducted; references obtained from these publications were subsequently reviewed for additional relevant articles.STUDY SELECTION AND DATA EXTRACTION:Representative clinical trials were summarized and relevant information was selected to assist in the understanding of VZV, the subsequent immune response, and the live-attenuated varicella vaccine.DATA SYNTHESIS:The physiologic, age-related decline in VZV cell–mediated immunity has been shown to be restored on administration of live-attenuated varicella vaccine. Various studies report serum anti-VZV antibody concentrations, and production of interferon-gamma were increased following vaccination. Concentrations subsequently returned to baseline one year after vaccination. Increase in responder cell frequency, a measure of cell-mediated immunity, has been reported to last up to four years after vaccination, at concentrations similar or superior to those observed following herpes zoster.CONCLUSIONS:Enhancement of cell-mediated immune response in elderly individuals through vaccination with live-attenuated varicella vaccine is a possible measure to protect this population from herpes zoster and to attenuate its complications. A summary of immunogenicity studies to identify the immune response to live-attenuated varicella vaccine in the elderly is presented. The absolute clinical significance, as well as appropriate administration guidelines of this prophylactic intervention, will become evident following forthcoming large, masked, placebo-controlled trials.
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Varicella-zoster virus (VZV) is a ubiquitous human pathogen that causes varicella, commonly called chicken pox; establishes latency; and reactivates as herpes zoster, referred to as shingles. A live attenuated varicella vaccine, derived from the Oka strain of VZV has clinical efficacy for the prevention of varicella. The vaccine induces persistent immunity to VZV in healthy children and adults. Immunization against VZV also has the potential to lower the risk of reactivation of latent virus. The varicella vaccine may eventually reduce or eliminate herpes zoster, which is a serious problem for elderly and immunocompromised individuals.
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