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To date, the pathogenesis of VZV infection is not fully understood because VZW is an exclusively human pathogen and is difficult to replicate in animal models (Breuer & Whitley, 2007).
Among immunocompromised populations, herpes zoster rashes typically are more severe and prolonged and may become disseminated, indicating VZV viremia. VZV rashes typically are presented by a well-defined dermatomal distribution in immunocompetent individuals, so the diagnosis can be established by characteristic clinical presentation. Acyclovir, famciclovir, and valacyclovir are nucleoside analogs that inhibit replication of human herpesviruses and are approved by the U.S.
Since VZV prophylaxis has been shown to effectively decrease the incidence of VZV reactivation and reduce disseminated VZV infection in BMT recipients, VZV prophylaxis should be considered for hematologic patients without BMT with severe myelosuppression.
Among high-risk patients without transplantation, reactivation and disseminated VZV infection also can occur.
However, the clinical presentation may be atypical or may have disseminated disease without rashes in immunocompromised patients; as a result, laboratory tests, including polymerase chain reaction, direct fluorescent antibody, and viral culture are needed to confirm the diagnosis.
Monitoring CD4 counts may be useful for clinicians in determining the need for VZV prophylaxis among high-risk populations, such as (a) hematologic patients with cancer following cytotoxic chemotherapy who fail to recover from myelosuppression over a prolonged period of time, (b) patients with myelodysplastic syndrome who have severe leukopenia refractory to granulocyte-colony-stimulating factor or granulocyte- macrophage-colony-stimulating factor, and (c) patients anticipating a prolonged course of immunosuppressive therapy who also are VZV seropositive (indicting a latent VZV state).
Two patients with solid cancers in the first author's practice developed disseminated VZV infections -- one patient with breast cancer receiving standard adjuvant chemotherapy and one patient with metastatic colorectal cancer who received chemotherapy over four years.
This clinical trial report, "Herpes Zoster (Shingles) Global Clinical Trials Review, H1, 2015," provides an overview of Herpes Zoster (Shingles) clinical trials scenario. Primary infection with VZV results in varicella or chickenpox, which largely affects children with a mild, self-limiting course (Wharton, 1996). Women have a slightly higher risk than men, and African Americans have a lower incidence of herpes zoster (Opstelten, Van Essen, Schellevis, Verheij, & Moons, 2006).


During initial viraemia, infected CD4 T cells cause down regulation of the histocompatibility complex class I expression and allow VZV to escape from the immune system (Ku, Padilla, Grose, Butcher, & Arvin, 2002). The most common rash sites are the thoracic and lumbar dermatomal zones (Yawn et al., 2007).
Therefore, considering VZV prophylaxis is clinically reasonable to reduce the risk of deadly disseminated VZV infection among high-risk patients with cancer without BMT. After clinical resolution of primary infection, viral latent infection is established when VZV retrogrades into the sensory dorsal roots of ganglia (Breuer & Whitley, 2007).
In addition, infected T cells transport VZV via T-cell trafficking from tonsillar tissue to the skin, where VZV replicates and produces cell-free VZV, resulting in highly infectious skin lesions. The rashes initially are erythematous and maculopapular, then progress to coalescing clusters of clear vesicles that contain high concentrations of VZV, which are contagious for VZV seronegative individuals. However, direct fluorescent antibody offers rapid diagnosis and is highly sensitive (Chan, Brandt, & Horsman, 2001). Therapy should be initiated within 72 hours of rash onset or as soon as possible (Dworkin et al.) (see Table 1). A retrospective analysis of 192 allogeneic peripheral blood stem cell transplantation recipients indicated that a very low dose of acylovir (200 mg daily) protected against VZV reactivation (Kim et al., 2008). In addition, the prophylaxis regimen may decrease patients' physical suffering and associated hospitalizations.
Vaccination in children to prevent primary VZV has reduced chickenpox cases in the United States (Marin, Guris, Chaves, Schmid, & Seward, 2007). Uninfected T cells also arrive at the infection sites, become primed with cell-free VZV, and mount a systemic immune response to control the initial infection (Ku et al., 2005).


In immunocompetent people, the rashes crust in 7-10 days and are no longer infectious (Harpaz et al., 2008).
The specimen is obtained by scraping the bases of uncrusted vesicular skin lesions and placing the scrapings on a plain glass slide.
Similarly, 137 BMT recipients who were given long-term acylovir of 200 mg daily until the end of immune suppression and at least one year following BMT had significantly decreased incidence of VZV reactivation, and visceral dissemination and serious complications were completely eliminated (Asano-Mori et al., 2008). Herpes zoster, the second clinical condition of VZV infection, results from the reactivation of this latent neurotropic virus and commonly presents with painful, unilateral vesicular skin eruption distributing within the dermatomal zones (Gnann & Whitley, 2002). Following initial infection, the VZV-specific cell-mediated immunity keeps VZV in latency and prevents its reactivation (Breuer & Whitley). Although VZV cutaneous dissemination may start with a dermatomal rash, it presents without any primary dermatomal involvement in some cases. When an individual's immune system is compromised, such as in older adults or people with cancer undergoing chemotherapy or transplantation, his or her VZV-specific cell mediated immunity also is likely to be impaired, leading to VZV reactivation. The most common complication following herpes zoster infection is postherpetic neuralgia, a persistent pain that can last months to years and occasionally becomes permanent. Adjunct therapy for pain and postherpetic neuralgia often is required for patients with herpes zoster.



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