Bocavirus viremia

Sukkaromdee, Pathoom; Wiwanitkit, Viroj

doi:10.4103/1817-1737.160848

Cited by 2 publications

(6 citation statements)

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“…Although findings were not similar among infected cats, the lymphotropic nature of FBoV is suggested as evidence of viral localization in lymphoid cells in all infected cases. Haematogenous spreading of bocaviruses has been speculated in several studies (Bonvicini et al., 2011; Sukkaromdee & Wiwanitkit, 2015) and was proposed as a significant cause of clinical symptoms corresponding to the affected organs where the virus was distributed to. The localization of FBoV in endothelial cells of small blood vessels in grey–white matter interface of brain stem, together with the presence of viral localization in non‐CNS tissue, may imply FBoV viremia.…”

Section: Discussionmentioning

confidence: 99%

“…Scale bar indicates nucleotide substitution per site.cases. Haematogenous spreading of bocaviruses has been speculated in several studies(Bonvicini et al, 2011;Sukkaromdee & Wiwanitkit, 2015) and was proposed as a significant cause of clinical symptoms corresponding to the affected organs where the virus was distributed to. The localization of FBoV in endothelial cells of small blood vessels in grey-white matter interface of brain stem, together with the presence of viral localization in non-CNS tissue, may imply FBoV viremia.Although a definitive statement regarding the causality of FBoV localization in brain could not be drawn, infection in brain cells resulting in neurologic deficits caused by this virus should be not underestimated.Interestingly, neuronal vacuolation is the common pathological feature found among FBoV-positive cats, and DNA labelling was also indicated in such vacuolated neurons.…”

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confidence: 99%

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Naturally acquired feline bocavirus type 1 and 3 infections in cats with neurologic deficits

Piewbang

Wardhani

Phongroop

et al. 2022

Transbounding Emerging Dis

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Feline bocaviruses (FBoVs) have been recognized as novel feline pathogens associated with gastrointestinal diseases. Although bocavirus infections in humans and animals present a broad range of clinical symptoms including neurologic diseases, the neuropathology caused by FBoV infection in cats is unknown. This study aims to investigate the presence of bocavirus in the brain samples of 78 cats showing neurologic deficits and 41 healthy cats using polymerase chain reaction (PCR) and to present the pathological findings of FBoV infection in brain tissues. Only five (6.41%, five out of 78) cats with neurological deficit were FBoV positive on PCR screening and were characterized as FBoV-1 (four out of five) and FBoV-3 (one out of five) by sequencing. Among FBoV-positive cases, viral DNA were detected by PCR in the cerebrum and brain stem of all FBoV-positive cases and rarely detected in the cerebellum of some cases.Histologically, all FBoV-positive cases revealed a variety of inflammatory responses. Among these, 80% (four out of five cases) showed multifocal neuronal vacuolation, mainly found in the cerebrum and brain stem. Eosinophilic inclusion-like materials were found within the nuclei of glial cells in the FBoV-3-positive case. In situ hybridization revealed FBoV DNA in oligodendroglia and vacuolated neurons detected using dual labelling with Olig-2 and NeuN immunohistochemistry, respectively. Transmission electron microscopy confirmed the presence of FBoV-3 virions in the nuclei of glial cells. Apart from localization in brain tissues, the FBoV DNA were also detected in multiple lymph nodes (five out of five) and some intestines (two out of five) of such positive cases, suggesting both parenteral and enteral infections. Complete genome sequence analysis revealed genetic diversity of detected FBoV-1, which were closely related to the strains found in China and Hong Kong, while the detected FBoV-3 presented distant monophyletic clade to previously detected FBoV-3 sequences. The FBoVs, together, should be considered a neurotropic virus and a possible cause for neuronal vacuolation in cats with neurologic deficits.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Naturally acquired feline bocavirus type 1 and 3 infections in cats with neurologic deficits

Piewbang

Wardhani

Phongroop

et al. 2022

Transbounding Emerging Dis

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“…Viremia induced by BoVs increases the possibility of dissemination of the virus to various organs and tissues [ 5 , 11 , 18 , 21 , 22 ]. If the virus can adapt to infect resident cells, novel tropism may result in infection of new cells.…”

Section: Discussionmentioning

confidence: 99%

“…However, we did not investigate the presence of CBoV-2 in blood of these cases, further investigations are needed to support this hypothesis. Evidence of viral hematogenous spreading of CBoV-2 and other BoVs has been reported, in addition to viral gene/genome detection in various organs [ 5 , 18 , 21 , 22 ]. The incongruence between our PCR and ISH data may be caused by a difference in sensitivity, as ISH has lower sensitivity than PCR [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have indicated that BoVs can cause viremia, which may lead to its detection in several organs via hematogenous spread [ 5 , 10 , 12 , 18 ]. If BoVs can enter the bloodstream and cause viremia, they may be able to disseminate to other parts of body [ 11 , 20 – 22 ] and/or localize and cause lesions [ 11 ]. As hematogenous spread is the typical route by which viruses enter organs, BoVs may be able to pass through the blood–brain barrier and cause lesions in the CNS [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

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Canine bocavirus-2 infection and its possible association with encephalopathy in domestic dogs

et al. 2021

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Canine bocaviruses (CBoVs) have been recognized as pathogens associated with intestinal diseases. Hematogenous spreading caused by CBoV has been documented and may potentiate the virus entry across the blood-brain barrier to initiate a brain infection. This study focused attention on CBoV detection in cases of encepahlopathy and attempted to determine its viral localization. A total of 107 dog brains that histologically exhibited encephalopathy (ED) were investigated for the presence of CBoVs using polymerase chain reaction (PCR). Thirty-three histologically normal brain samples from dogs were used as a control group (CD). CBoV-2 was detected in 15 ED dogs (14.02%) but not in CD dogs (p = 0.02), while no CBoV-1 and -3 were detected. Among the CBoV-2 positive dogs, brain histological changes were characterized by nonsuppurative encephalitis, with inclusion body-like materials in some brains. In situ hybridization (ISH) and transmission electron microscopy (TEM) confirmed the presence of CBoV-2 viral particles in glial cells, supporting neurotropism of this virus. ISH signals were also detected in the intestines, lymphoid organs, and the heart, suggesting both enteral and parenteral infections of this virus. Whole genome characterization and evolutionary analysis revealed genetic diversity of CBoV-2 sequences and it was varying among the different countries where the virus was detected. This study points to a possible association of CBoV-2 with encephalopathy in dogs. It also highlights the genetic diversity and cellular tropism of this virus.

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Bocavirus viremia

Cited by 2 publications

References 5 publications

Naturally acquired feline bocavirus type 1 and 3 infections in cats with neurologic deficits

Naturally acquired feline bocavirus type 1 and 3 infections in cats with neurologic deficits

Canine bocavirus-2 infection and its possible association with encephalopathy in domestic dogs

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