Yaba poxvirus disease
Yaba poxvirus disease
Description, Causes and Risk Factors:
The poxvirus (genus Orthopoxvirus) used in the immunization of people against variola (smallpox), usually causing a local reaction but sometimes generalized vaccinia, especially in children; the virus is closely related serologically to the viruses of variola and cowpox, but certain differences have been demonstrated which indicate that they are perhaps distinct but closely related strains of a variola-vaccinia-cowpox complex; the lineage of poxvirus is uncertain, and it is very unlikely that it descended from Jenner original virus.
A poxvirus was identified by Andrewes as the etiologic agent responsible for an outbreak of subcutaneous tumors in 1956 among a colony of rhesus monkeys housed in Yaba, Nigeria. The virus, now known as Yaba tumor poxivirus, has been found to be infectious for man. The tumors have been identified as benign histiocytomas.
The poxviruses are the largest known DNA viruses and are distinguished from other viruses by their ability to replicate entirely in the cytoplasm of infected cells. Poxviruses do not require nuclear factors for replication and, thus, can replicate with little hindrance in enucleated cells.
Infectious viral particles contain many of the enzymes necessary for replication within the virion itself, hence the large size of the virus. Because of its size, poxvirus was the first animal virus observed using microscopy. Specific enzymes, including DNA-dependent RNA polymerase, polyA polymerase, and several capping enzymes are all packaged within the core of the virus. The core also contains a 200-kilobase (kb), double-stranded DNA genome and is surrounded by a lipoprotein core membrane.
The life cycle of poxvirus begins when the virus fuses with the plasma membrane of a susceptible cell via a protein-based entry-fusion complex or is absorbed by cellular endosomes (A more or less central body in the vesicular nucleus of certain Feulgen-negative (DNA-) protozoa (e.g., trypanosomes, parasitic amebae, and phytoflagellates), with the chromatin (DNA+) lying between the nuclear membrane and the endosome). No specific receptor used to facilitate entry into the cell has yet been discovered. Once the virus has entered the cell, the viral core is released into the cytoplasm of the cell, where virally packaged transcriptases initiate transcription of early genes.
The virus replicates in primary cultures of rhesus, cynomologous cercopithecus, and human embryonic cells, but is best grown and titrated in continuous cercopithecus kidney cell lines or in cynomologous kidney cell lines. Although Yaba virus resembles the vacinia subgroup of poxviruses morphologically, it appears to be only remotely related serologically. No cross-protection to Yaba virus is afforded monkeys immunized with vaccinia virus or related monkey poxviruses and vice versa. By immunodiffusion, convalescent Yaba monkey sera yield a single weak precipitin line with vaccinia nucleoprotein (NP) antigen, a reaction indicative of the presence of the poxvirus NP group antigen in Yaba poxvirus.
Most patients who are administered poxvirus experience mild pain and pruritus at the site of injection that lasts about 7-10 days. During this time, patients may also develop regional lymphadenopathy and low-grade fever, which usually resolves without intervention.Complications that are more serious also can occur in patients with predisposing risk factors. A history of eczema, CNS disease, or immunosuppression places the patient at high risk for developing a serious complication if exposed to the virus.
The diagnosis of poxvirus complications is usually straightforward and depends on obtaining the history of recent poxvirus exposure by vaccination or contact with a vaccinated individual. A careful workup for immune deficiency should be considered in patients who do not promptly improve.
The diagnosis of CNS complications is more difficult because the signs and symptoms are nonspecific. Although rare, postvaccinial encephalitis should be considered in any patient with neurologic symptoms developing 1-2 weeks after exposure to live poxvirus.Poxvirus has not been isolated from cerebrospinal fluid (CSF) of patients with encephalitis, and CSF analysis usually produces normal results, except for increased pressure; however, CSF analysis may be indicated to exclude other causes of encephalitis.
Treatment for the complications associated with poxvirus is supportive.
VIG may be helpful in selected patients, such as those with generalized poxvirus and eczema vaccinatum or those at high risk for developing complications following vaccination with poxvirus. VIG is less successful when used for treatment of progressive poxvirus and CNS complications. VIG was developed from pooled sera collected from vaccinated patients in the 1960s and is available from the Centers for Disease Control and Prevention (CDC) in Atlanta, GA. VIG is contraindicated in patients with allergies to VIG or sensitivity to human pooled serum.
Cidofovir and adefovir are being investigated to evaluate the clinical effect and outcomes as a secondary treatment of poxvirus-related complications that do not respond to VIG treatment. An oral form of this drug is currently under development.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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