PCR detected hepatitis C virus genome in the brain of a case with progressive encephalomyelitis with rigidity

Bolay, Hayrünnisa; Söylemezoğlu, Figen; Nurlu, Gülay; Tunçer, Serdar; Vari, Kubilay

doi:10.1016/0303-8467(96)00040-6

Cited by 80 publications

(66 citation statements)

References 10 publications

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“…41 Again, however, contradictory data have been reported: immunohistochemistry has failed to stain non-structural HCV proteins in the skin of cryoglobulinemic, chronic hepatitis C patients, 42 and a careful RT-PCR study has suggested the absence of HCV RNA in salivary gland epithelial cells. 43 Finally, the presence of HCV in the brain has only been anecdotally reported 44 and awaits confirmation.…”

mentioning

confidence: 98%

Does the hepatitis C virus replicate in cells of the hematopoietic lineage?

Negro

Levrero

1998

Hepatology

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mentioning

confidence: 98%

Does the hepatitis C virus replicate in cells of the hematopoietic lineage?

Negro

Levrero

1998

Hepatology

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“…HCV infection has been correlated to numerous neuro logical disorders ranging from meningeal to encephalic inflammation and leukoencephalitis [17,18] . Clinically a wide range of complications have been associated with HCV infection, ranging from encepha lomyelitis to loss of neurons though sphincter impair ment, spastic quadriparesis and sensory dominate the clinically know complication [17] .…”

Section: Cns Involvement In Hcv Infectionmentioning

confidence: 99%

Hepatitis C virus and neurological damage

Mathew

Faheem

Ibrahim

et al. 2016

WJH

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Author contributions: Mathew S and Faheem M contributed equally to this manuscript; Qadri I conceived and designed the topic; Mathew S, Faheem M, Ibrahim SM, Iqbal W and Rauff B contributed to materials and wrote the paper; Faheem M, Ibrahim SM, Iqbal W, Rauff B, Fatima K and Qadri I contributed to proof reading of the manuscript.Supported by KACST large R and D grant to Ishtiaq Qadri (#162-34).Conflict-of-interest statement: Authors declare no conflict of interests for this article. AbstractChronic hepatitis C virus (HCV) infection exhibits a wide range of extrahepatic complications, affecting various organs in the human body. Numerous HCV patients suffer neurological manifestations, ranging from cognitive impairment to peripheral neuropathy. Overexpression of the host immune response leads to the production of immune complexes, cryoglobulins, as well as autoantibodies, which is a major pathogenic mechanism responsible for nervous system dysfunction. Alternatively circulating inflammatory cytokines and chemokines and HCV replication in neurons is another factor that severely affects the nervous system. Furthermore, HCV infection causes both sensory and motor peripheral neuropathy in the mixed cryoglobulinemia as well as known as an important risk aspect for stroke. These extrahepatic manifestations are the reason behind underlying hepatic encephalopathy and chronic liver disease. The brain is an apt location for HCV replication, where the HCV virus may directly wield neurotoxicity. Other mechanisms that takes place by chronic HCV infection due the pathogenesis of neuropsychiatric disorders includes derangement of metabolic pathways of infected cells, autoimmune disorders, systemic or cerebral inflammation and alterations in neurotransmitter circuits. HCV and its pathogenic role is suggested by enhancement of psychiatric and neurological symptoms in patients attaining a sustained virologic response followed by treatment with interferon; however, further studies are required to fully assess the impact of HCV infection and its specific antiviral targets associated with neuropsychiatric disorders. REVIEWSubmit a

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“…This is consistent with prior literature, in which HCV has not generally been associated with encephalitis or myelitis. Only rare case reports have described individuals with acute inflammatory syndromes involving brain or spinal cord, in which HCV RNA has been demonstrated in brain or CSF (Bolay et al, 1996;Fujita et al, 1999;Gazzola et al, 2001;Sacconi et al, 2001). A caveat with our analysis is that it was performed only through light microscopic examination of routine H&E stains, and thus only pronounced accumulations of inflammatory cells would have been appreciated.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathologic correlates of hepatitis C virus in brain: A pilot study

et al. 2008

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Hepatitis C virus (HCV) has been detected in the brain tissues of 10 individuals reported to date; it is unclear what clinical factors are associated with this, and with what frequency it occurs. Accordingly, a pilot analysis utilizing reverse transcriptase-polymerase chain reaction (RT-PCR) to detect and sequence HCV in premortem plasma and postmortem brain and liver from 20 human immunodeficiency virus (HIV)-infected and 10 HIV-naïve individuals was undertaken. RNA encoding the first 126 amino acids of the HCV E1 envelope protein and the majority of the E1 signal sequence was analyzed in parallel with an 80-base-long segment of the 5′ untranslated region (UTR). Liver HCV was detected only in subjects with premortem HCV viremia (10 HIV-infected and 3 HIVnaïve). Brain HCV was detected in 6/10 HCV/HIV-coinfected and 1/3 HCV-monoinfected subjects. In the setting of HIV, the magnitude of plasma HCV load did not correlate with the presence of brain HCV. However, coinfected patients with brain HCV were more often off antiretroviral therapy and tended to have higher plasma HIV loads than those with HCV restricted to liver. Furthermore, premortem cerebrospinal fluid (CSF) analysis revealed that HCV/HIV-coinfected patients with brain HCV had detectable CSF HIV, whereas those without brain HCV had undetectable CSF HIV loads (P = .0205). Neuropsychologic tests showed a trend for hierarchical impairment of abstraction/ executive functioning in HIV/HCV coinfection, with mean T scores for HIV monoinfected patients 43.2 (7.3), for liver-only HCV 39.5 (9.0), and for those with HCV in brain and liver 33.2 (5.1) (P = . 0927). Predominant brain HCV sequences did not match those of the plasma or liver in 4 of the 6 coinfected patients analyzed. We conclude that in the setting of HIV/HCV coinfection, brain HCV is a common phenomenon unrelated to the magnitude of HCV viremia, but related to active HIV disease and detectable CSF HIV. Furthermore, there is sequence evidence of brain compartmentalization. Differences in abstraction/executive function of HCV/HIV coinfected patients compared to HIV monoinfected warrant further studies to determine if neuropsychiatric effects are predicated upon brain infection.

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PCR detected hepatitis C virus genome in the brain of a case with progressive encephalomyelitis with rigidity

Cited by 80 publications

References 10 publications

Does the hepatitis C virus replicate in cells of the hematopoietic lineage?

Does the hepatitis C virus replicate in cells of the hematopoietic lineage?

Hepatitis C virus and neurological damage

Clinicopathologic correlates of hepatitis C virus in brain: A pilot study

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