Primary VZV infection generally occurs in childhood and is usually mild but complications can occur in adults and in immunocompromised patients. Clinical Characteristics of VZV Infections The narrow host range (VZV infection is highly restricted to humans) coupled with the highly cell-associated nature of the virus, has hampered the development of a reliable animal model that mimics VZV diseases in human, thereby hindering VZV pathogenesis studies.Ģ. Risks factors for HZ include older age, CMI dysfunction, diabetes, female gender, genetic susceptibility, physical trauma, recent psychological stress, and white race. Reactivation from latency occurs when there is a weakening in cell-mediated immunity (CMI) as a natural consequence of aging since VZV-specific T cells lose their ability to proliferate with age or with immune suppression.
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The virus can also be transmitted by fomites from varicella and shingles skin lesions. This gives a skin rash within the dermatome innervated by a single sensory nerve. During VZV reactivation, the virus is transported along microtubules within sensory axons to infect epithelial cells, usually without viremia. In most individuals, VZV infection results in lifelong immunity. After 10–21 days, the virus arrives at the skin, producing the typical vesicular rash characteristic of varicella. VZV is highly infectious and enters the body via the respiratory tract, followed by rapid spread from the pharyngeal lymphoid tissue to circulating T lymphocytes. Herpes zoster (HZ) is characterized by a localized rash in a unilateral, dermatomal distribution and is often associated with severe neuropathic pain. VZV reactivation produces skin lesions characteristic of herpes zoster (shingles), causing significant morbidity, but rarely mortality. During latency, the viral DNA persists in the dorsal root ganglia and cranial root ganglia. Like all herpesviruses, VZV undergoes a lifelong latent state following primary infection. VZV is the causative agent of chickenpox (varicella), a common infantile illness. VZV together with herpes simplex virus 1 and 2 (HSV-1 and HSV-2) belong to the α-herpesvirinae, characterized by establishment of latency in neurons. The herpesvirus family includes three subfamilies, α, β, and γ-herpesvirinae. Varicella-zoster virus (VZV), also known as human herpesvirus 3 (HHV-3) has a double-stranded DNA genome of 125 kb, encoding for approximately 71 open reading frames (ORFs). Their low efficacy in controlling HZ pain and post-herpetic neuralgia development, and the need of multiple dosing regimens requiring daily dose adaptation for patients with renal failure urges the development of novel anti-VZV drugs. We reflect on the role of antiviral agents in the treatment of VZV-associated diseases, as a large percentage of the at-risk population is not immunized, and on the limitations of currently FDA-approved anti-VZV drugs. Valnivudine hydrochloride (FV-100) and valomaciclovir stearate (in advanced stage of development) and several new molecules potentially good as anti-VZV candidates described during the last year are examined. We also focus on acyclovir, valacyclovir, and famciclovir (FDA approved drugs to treat VZV infections), brivudine (used in some European countries) and amenamevir (a helicase-primase inhibitor, approved in Japan) that augur the beginning of a new era of anti-VZV therapy.
We discuss VZV diseases and the decrease in their incidence due to the introduction of live-attenuated vaccines to prevent varicella or HZ. The virus can reactivate, causing herpes zoster (HZ, shingles) and leading to significant morbidity but rarely mortality, although in immunocompromised hosts, VZV can cause severe disseminated and occasionally fatal disease. Varicella-zoster virus (VZV), a common and ubiquitous human-restricted pathogen, causes a primary infection (varicella or chickenpox) followed by establishment of latency in sensory ganglia.
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