Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25623836
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25623836
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Ann+Neurol
2015 ; 77
(4
): 560-70
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Persistence and pathogenesis of the neurotropic polyomavirus JC
#MMPMID25623836
Wollebo HS
; White MK
; Gordon J
; Berger JR
; Khalili K
Ann Neurol
2015[Apr]; 77
(4
): 560-70
PMID25623836
show ga
Many neurological diseases of the central nervous system (CNS) are underpinned by
malfunctions of the immune system, including disorders involving opportunistic
infections. Progressive multifocal leukoencephalopathy (PML) is a lethal CNS
demyelinating disease caused by the human neurotropic polyomavirus JC (JCV) and
is found almost exclusively in individuals with immune disruption, including
patients with human immunodeficiency virus/acquired immunodeficiency syndrome,
patients receiving therapeutic immunomodulatory monoclonal antibodies to treat
conditions such as multiple sclerosis, and transplant recipients. Thus, the
public health significance of this disease is high, because of the number of
individuals constituting the at-risk population. The incidence of PML is very
low, whereas seroprevalence for the virus is high, suggesting infection by the
virus is very common, and so it is thought that the virus is restrained but it
persists in an asymptomatic state that can only occasionally be disrupted to lead
to viral reactivation and PML. When JCV actively replicates in oligodendrocytes
and astrocytes of the CNS, it produces cytolysis, leading to formation of
demyelinated lesions with devastating consequences. Defining the molecular nature
of persistence and events leading to reactivation of the virus to cause PML has
proved to be elusive. In this review, we examine the current state of knowledge
of the JCV life cycle and mechanisms of pathogenesis. We will discuss the normal
course of the JCV life cycle including transmission, primary infection, viremia,
and establishment of asymptomatic persistence as well as pathogenic events
including migration of the virus to the brain, reactivation from persistence,
viral infection, and replication in the glial cells of the CNS and escape from
immunosurveillance.