Detection of intrathecal IgM, IgG and IgA in a Cuban West Nile virus confirmed case

Pupo-Antúnez, Maritza; Dorta‐Contreras, Alberto Juan; Vazquez, Yaimee; González-Hernández, Marlen; Noris-García, Elena; Padilla-Docal, Bárbara; Bu-Coifiu-Fanego, Raisa

doi:10.1590/s0004-282x2008000400030

Cited by 1 publication

(3 citation statements)

References 16 publications

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“…West Nile virus immunoglobulin M (IgM) in human CSF (Alpert, Fergeson & Noel 2003;Pupo-Antunez et al 2008) and in human neonates (Alpert et al 2003) is considered to be diagnostic of WNV infection, since IgM passes neither the blood brain barrier (BBB) nor the placenta. Studies in horses with naturally occurring WNV encephalitis (Ostlund et al 2001;Porter 2004) showed low levels of CSF WNV IgM compared with high serum levels in the presence of an intact BBB.…”

Section: Discussionmentioning

confidence: 99%

“…Studies in horses with naturally occurring WNV encephalitis (Ostlund et al 2001;Porter 2004) showed low levels of CSF WNV IgM compared with high serum levels in the presence of an intact BBB. A human, Mexican patient with fatal WNV was shown to produce IgM, IgG and IgA, in decreasing order of concentration, intrathecally within the CNS and not due to disruption of the BBB (Pupo-Antunez et al 2008). Intrathecal Ig synthesis is originated by perivascular infiltrations of B-lymphocytes, which are locally matured and can be associated with CNS diseases (Porter 2004;Pupo-Antunez et al 2008).…”

Section: Discussionmentioning

confidence: 99%

“…A human, Mexican patient with fatal WNV was shown to produce IgM, IgG and IgA, in decreasing order of concentration, intrathecally within the CNS and not due to disruption of the BBB (Pupo-Antunez et al 2008). Intrathecal Ig synthesis is originated by perivascular infiltrations of B-lymphocytes, which are locally matured and can be associated with CNS diseases (Porter 2004;Pupo-Antunez et al 2008). In the current series of horses, CSF was not sampled for WNV IgM testing; however, had it been found to be IgM positive, its presence could have been explained by the presence of the few-to-several B-lymphocytes and plasma cells, as labelled by CD20 and MUM1 IHC in the CNS sections.…”

Section: Discussionmentioning

confidence: 99%

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Pathology of fatal lineage 1 and 2 West Nile virus infections in horses in South Africa

Williams¹,

Niekerk²,

Human³

et al. 2014

J S Afr Vet Assoc

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Since 2007, West Nile virus (WNV) has been reported in South African horses, causing severe neurological signs. All cases were of lineage 2, except for one case that clustered with lineage 1 viruses. In the present study, gross and microscopic lesions of six South African lineage 2-infected horses and the one lineage 1 case are described. Diagnoses were confirmed by real-time reverse-transcriptase polymerase chain reaction (RT-PCR) of central nervous system (CNS) tissue and one by RT-PCR of a brain virus isolate. The CNS of all cases was negative by RT-PCR or immunohistochemistry (IHC) for African horse sickness (AHS), equine encephalosis virus, equine herpes viruses 1 and 4, other zoonotic flaviviruses, alphaviruses, and shunivirus, and either by immunofluorescence or IHC for rabies. Gross visceral lesions were nonspecific but often mimicked those of AHS. The CNS histopathology of WNV lineage 2 cases resembled the nonsuppurative polioencephalomyelitis reported in the Northern Hemisphere lineage 1 and recent Hungarian lineage 2 cases. Occasional meningitis, focal spinal ventral horn poliomalacia, dorsal and lateral horn poliomyelitis, leucomyelitis, asymmetrical ventral motor spinal neuritis and frequent olfactory region involvement were also seen. Lineage 2 cases displayed marked variations in CNS lesion severity, type and distribution, and suggested various viral entry routes into the CNS, based on findings in experimental mice and hamsters. Lineage 1 lesions were comparable to the milder lineage 2 cases. West Nile virus IHC on CNS sections with marked lesions from all cases elicited only two antigen-positive cells in the olfactory cortex of one case. The presence in the CNS of T-lymphocytes, B-lymphocytes, plasma cells and macrophage-monocytes was confirmed by cluster of differentiation (CD) 3, CD20, multiple myeloma oncogene 1 (MUM1) and macrophage (MAC) 387 IHC.

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