Cell death in bovine parvovirus-infected embryonic bovine tracheal cells is mediated by necrosis rather than apoptosis

Abstract

Cell death in bovine parvovirus-infected embryonic bovine tracheal cells is mediated by necrosis rather than apoptosis The helper-independent bovine parvovirus (BPV) was studied to determine its effect on host embryonic bovine tracheal (EBTr) cells: whether the ultimate outcome of infection results in apoptotic cell death or cell death by necrosis. Infected cells were observed for changes marking apoptosis. Observations of alterations in nuclear morphology, membrane changes, apoptotic body formation, membrane phosphatidylserine inversions, caspase activation and cell DNA laddering in infected cells were not indicative of apoptosis. On the other hand, at the end of the virus replication cycle, infected cells released viral haemagglutinin and infectious virus particles, as would be expected from cell membrane failure. Moreover, the infected cells released lactate dehydrogenase (LDH), release of which is a marker of necrosis. LDH release into the cell medium correlated directly with viral m.o.i. and time post-infection. Furthermore, assessment of mitochondrial dehydrogenase activity was consistent with cell death by necrosis. Taken together, these findings indicate that cell death in BPV-infected EBTr cells is due to necrosis, as defined by infected-cell membrane failure and release of the cell contents into the extracellular environment.

Bovine parvovirus uses clathrin-mediated endocytosis for cell entry

“…In a preponderance of infected cells, the virus must wait for the cell to enter the S phase before viral genome replication and transcription can occur. Moreover, progeny virus is released from infected cells by necrosis (Abdel-Latif et al, 2006), a process during which new virus is waiting to be released. Thus, there were probably no secondary foci of antigen-positive cells to confound the cell-number counts at 48 h post-infection.…”

Bocavirus Infection in Children at the Current Stage. A Literature Review

“…Далее вирион посредством кла-трин-опосредованного эндоцитоза проникает в клетку, по системе микротрубочек транспортируется к ядру, затем вирусный одноцепочечный геном проникает в ядро. Дочерние одноцепочечные ДНК могут быть превра-щены в двухцепочечные и участвовать в новых атаках транскрипции и репликации, а так же могут быть упакова-ны в новые вирионы, которые высвобождаются из клетки-хозяина [17]. По результатам сероэпидемиологических исследований, проведенных в Японии и США, практиче-ски все дети старше 6 лет (60-100%) и почти все взрос-лые (94-100%) имели антитела к бокавирусу [12,13,25].…”

Clathrin-Associated Endocytosis as a Route of Entry into Cells for Parvoviruses

“…Although the purpose of this review is to only take the entering virus to the intranuclear environment, it is interesting to note that in CPV infection the nuclear replication compartment expands and is accompanied by chromatin marginalization to the vicinity of the nuclear membrane, virus capsids move by passive diffusion, intranuclear structure and dynamics are extensively affected enlarging the interchromosomal domain which contains viral proteins, genomes, and capsids (Ihalainen et al, 2009). After parvovirus assembly and maturation within the nucleus of infected cells, they egress by processes that include apoptosis (Poole et al, 2004;Poole et al, 2006) and cell necrosis (Abdel-Latif et al, 2006).…”