The Capsid Proteins of Aleutian Mink Disease Virus Activate Caspases and Are Specifically Cleaved during Infection

Cheng, Fang; Chen, Aaron Yun; Best, Sonja M.; Bloom, Marshall E.; Pintel, David J.; Qiu, Jianming

doi:10.1128/jvi.01917-09

Cited by 30 publications

(30 citation statements)

References 51 publications

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“…Cleaved NS1 helps to replicate the viral genome (9). Thus, a low level of DNA replication during the permissive mode of infection is a result of a balance between the stimulatory role of cleaved NS1 and the inhibitory role of cleaved capsid protein (limiting packaging of the single-stranded viral genome) (9). The health status of the mink from the two farms described in the present work is the consequence of both restricted and permissive modes of infection.…”

Section: Discussionmentioning

confidence: 82%

Effect of Persistent Infection of Mink with Aleutian Mink Disease Virus on Reproductive Failure

Reichert

Kostro

2014

Bulletin of the Veterinary Institute in Pulawy

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The aim of this study was to assess the impact of asymptomatic infections of mink with Aleutian mink disease virus (AMD on reproductive performance and the morphology of the internal organs. The study drew its subjects from two farms where the disease was endemic and included 450 clinically healthy female mink divided into three equal groups: two AMD positive groups and one AMD negative control group. The mink were subjected to clinical observations throughout the period of reproduction, and then for the first seven weeks after birth. Data collected during this period were evaluated using selected breeding and reproductive indices. All reproductive indices including conception rate, litter size, and litter weight at birth as well as neonatal mortality were substantially poorer. Histopathological examination revealed changes typical for AMD, particularly in the spleen, kidneys, liver, and lymph nodes. The results highlighted and proved the frequently underestimated extent of economic losses on farms where AMD is endemic yet the mink stock is apparently healthy.

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Section: Discussionmentioning

confidence: 82%

Effect of Persistent Infection of Mink with Aleutian Mink Disease Virus on Reproductive Failure

Reichert

Kostro

2014

Bulletin of the Veterinary Institute in Pulawy

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“…One attractive explanation might be that cleavage of the capsid proteins occurs as part of the disassembly process. However, SV40 capsid proteins do not appear to be cleaved by caspases, as found for other viruses such as influenza virus (63), feline calicivirus (2), and Aleutian mink disease virus (16). Caspase cleavage sites were not identified by bioinformatics analysis, and cleavage of the capsid proteins was not detected by Western analysis, suggesting a different role for caspases in SV40 infection.…”

Section: Activation Of Parp-1mentioning

confidence: 79%

Simian Virus 40 Infection Triggers a Balanced Network That Includes Apoptotic, Survival, and Stress Pathways

Butin‐Israeli¹,

Drayman²,

Oppenheim³

2010

J Virol

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The infection process by simian virus 40 (SV40) and entry of its genome into nondividing cells are only partly understood. Infection begins by binding to GM1 receptors at the cell surface, cellular entry via caveolar invaginations, and trafficking to the endoplasmic reticulum, where the virus disassembles. To gain a deeper insight into the contribution of host functions to this process, we studied cellular signaling elicited by the infecting virus. Signaling proteins were detected by Western blotting and immunofluorescence staining. The study was assisted by a preliminary proteomic screen. The contribution of signaling proteins to the infection process was evaluated using specific inhibitors. We found that CV-1 cells respond to SV40 infection by activating poly(ADP-ribose) polymerase 1 (PARP-1)-mediated apoptotic signaling, which is arrested by the Akt-1 survival pathway and stress response. A single key regulator orchestrating the three pathways is phospholipase C-gamma (PLC␥). The counteracting apoptotic and survival pathways are robustly balanced as the infected cells neither undergo apoptosis nor proliferate. Surprisingly, we have found that the apoptotic pathway, including activation of PARP-1 and caspases, is absolutely required for the infection to proceed. Thus, SV40 hijacks the host defense to promote its infection. Activities of PLC␥ and Akt-1 are also required, and their inhibition abrogates the infection. Notably, this signaling network is activated hours before T antigen is expressed. Experiments with recombinant empty capsids, devoid of DNA, indicated that the major capsid protein VP1 alone triggers this early signaling network. The emerging robust signaling network reflects a delicate evolutionary balance between attack and defense in the host-virus relationship.

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“…4B). However, it is also possible that the band of ~90 kDa was a cleaved product of the VP1 protein of 101 kDa, since the capsid proteins of other parvoviruses have been reported to be cleaved (Farr et al, 2006; Cheng et al, 2009). …”

Section: Resultsmentioning

confidence: 99%

Molecular characterization of the newly identified human parvovirus 4 in the family Parvoviridae

Lou

Huang

et al. 2012

Virology

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Human parvovirus 4 (PARV4) is an emerging human virus, and little is known about the molecular aspects of PARV4 apart from its incomplete genome sequence, which lacks information of the termini. We analyzed the gene expression profile of PARV4 using a nearly full-length HPV4 genome in a replication competent system in 293 cells. We found that PARV4 utilizes two promoters to transcribe non-structural protein- and structural protein-encoding mRNAs, respectively, which were polyadenylated at the right end of the genome. Three major proteins, including the large non-structural protein NS1a, whose mRNA is spliced, and capsid proteins VP1 and VP2, were detected. Additional functional analysis of the NS1a revealed its capability to induce cell cycle arrest at G2/M phase in ex vivo-generated human hematopoietic stem cells. Taken together, our characterization of the molecular features of PARV4 suggests that PARV4 represents a new genus in the family Parvoviridae.

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The Capsid Proteins of Aleutian Mink Disease Virus Activate Caspases and Are Specifically Cleaved during Infection

Abstract: Aleutian mink disease virus (AMDV) is currently the only known member of the genus

Cited by 30 publications

References 51 publications

Effect of Persistent Infection of Mink with Aleutian Mink Disease Virus on Reproductive Failure

Effect of Persistent Infection of Mink with Aleutian Mink Disease Virus on Reproductive Failure

Simian Virus 40 Infection Triggers a Balanced Network That Includes Apoptotic, Survival, and Stress Pathways

Molecular characterization of the newly identified human parvovirus 4 in the family Parvoviridae

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