The fight of viruses against apoptosis

Institut für Klinische und Molekulare Virologie, Schlossgarten 4, D-91054 Erlangen, Germany
Current Opinion in Genetics & Development (Impact Factor: 7.57). 02/1998; 8(1):82-87. DOI: 10.1016/S0959-437X(98)80066-X


The induction of apoptosis of virus-infected cells is an important host defense mechanism against invading pathogens. Some viruses express anti-apoptotic proteins that efficiently block apoptosis induced by death receptors or in response to stress signaled through mitochondria. Viral interference with host cell apoptosis leads to enhanced viral replication and may promote cancer.

3 Reads
  • Source
    • "targets the induction of apoptosis in infected cells which, when it occurs early in the infection, prevents viral replication and distribution (Hay and Kannourakis, 2002). The viral strategy can, for example, result in the inhibition of cellular apoptosis to ensure viral replication in the host cells, or the active induction of apoptosis in order to impair the immune response or to release progeny at the later stage of viral replication (Best and Bloom, 2004; Leu et al., 2013; Tschopp et al., 1998). The association between apoptosis and viral infection is therefore complex, either increasing or reducing host cell death. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Whilst Herpesviridae, which infect higher vertebrates, actively influence host immune responses to ensure viral replication, it is mostly unknown if Alloherpesviridae, which infect lower vertebrates, possess similar abilities. An important antiviral response is clearance of infected cells via apoptosis, which in mammals influences the outcome of infection. Here, we utilise common carp infected with CyHV-3 to determine the effect on the expression of genes encoding apoptosis-related proteins (p53, Caspase 9, Apaf-1, IAP, iNOS) in the pronephros, spleen and gills. The influence of CyHV-3 on CCB cells was also studied and compared to SVCV (a rhabdovirus) which induces apoptosis in carp cell lines. Although CyHV-3 induced iNOS expression in vivo, significant induction of the genetic apoptosis pathway was only seen in the pronephros. In vitro CyHV-3 did not induce apoptosis or apoptosis-related expression whilst SVCV did stimulate apoptosis. This suggests that CyHV-3 possesses mechanisms similar to herpesviruses of higher vertebrates to inhibit the antiviral apoptotic process.
    Veterinary Microbiology 12/2014; DOI:10.1016/j.vetmic.2014.12.012 · 2.51 Impact Factor
  • Source
    • "Interference with apoptosis by inhibiting the proteolytic activity of cysteine aspartic acid proteases (caspases) prolongs the life of virus-infected cells, resulting in enhanced viral replication and viral persistence [4]. Caspases are a family of structurally related cysteine proteases, and they play a central role in apoptosis. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Apoptosis plays an important role in white spot syndrome virus (WSSV) pathogenesis, and caspases are central players in apoptosis. Here, we cloned four novel caspases (Lvcaspase2-5) from the Pacific white shrimp Litopenaeus vannamei, and investigated their potential roles in WSSV replication using dsRNA-mediated gene silencing. Lvcaspase2-5 have the typical domain structure of caspase family proteins, with the conserved consensus motifs p20 and p10. Lvcaspase2 and Lvcaspase5 were highly expressed in muscle, while Lvcaspase3 was highly expressed in hemocytes and Lvcaspase4 was mainly expressed in intestine. Lvcaspase2-5 could also be upregulated by WSSV infection, and they showed different patterns in various tissues. When overexpressed in Drosophila S2 cells, Lvcaspase2-5 showed different cellular localizations. Using dsRNA-medicated gene silencing, the expression of Lvcaspase2, Lvcaspase3, and Lvcaspase5 were effectively knocked down. In Lvcaspase2-, Lvcaspase3- or Lvcaspase5-silenced L. vannamei, expression of WSSV VP28 gene was significantly enhanced, suggesting protective roles for Lvcaspase2, Lvcaspase3 and Lvcaspase5 in the host defense against WSSV infection.
    PLoS ONE 12/2013; 8(12):e80418. DOI:10.1371/journal.pone.0080418 · 3.23 Impact Factor
  • Source
    • "Apoptosis is a tightly regulated process in which excess or damaged cells are eliminated to maintain tissue homeostasis [1,3,6,21]. Apoptosis is also a major defense mechanism to remove unwanted and potentially dangerous cells, such as virus-infected cells [3,5,54,55]. Shrimps use apoptosis in defense against WSSV infection, and WSSV encodes two anti-apoptosis proteins, AAP-1 (ORF390 or WSSV449) and WSSV222, to subvert host apoptosis responses to facilitate viral replication [26,27,29,39]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Inhibitors of apoptosis (IAPs) play important roles in apoptosis and NF-κB activation. In this study, we cloned and characterized three IAPs (LvIAP1-3) from the Pacific white shrimp, Litopenaeusvannamei. LvIAP1-3 proteins shared signature domains and exhibited significant similarities with other IAP family proteins. The tissue distributions of LvIAP1-3 were studied. The expression of LvIAP1-3 was induced in the muscle after white spot syndrome virus (WSSV) infection. LvIAP1 expression in the gill, hemocytes, hepatopancreas, and intestine was responsive to WSSV and Vibrioalginolyticus infections. LvIAP2 expression in the gill, hemocytes, and hepatopancreas was also responsive to WSSV infection. The expression of LvIAP3 in the gill, hemocytes, and intestine was reduced after V. alginolyticus infection. When overexpressed in Drosophila S2 cells, GFP labeled-LvIAP2 was distributed in the cytoplasm and appeared as speck-like aggregates in the nucleus. Both LvIAP1 and LvIAP3 were widely distributed throughout the cytoplasm and nucleus. The expression of LvIAP1, LvIAP2, and LvIAP3 was significantly knocked down by dsRNA-mediated gene silencing. In the gill of LvIAP1- or LvIAP3-silenced shrimp, the expression of WSSV VP28 was significantly higher than that of the dsGFP control group, suggesting that LvIAP1 and LvIAP3 may play protective roles in host defense against WSSV infection. Intriguingly, the LvIAP2-silenced shrimp all died within 48 hours after dsLvIAP2 injection. In the hemocytes of LvIAP2-silenced shrimps, the expression of antimicrobial peptide genes (AMPs), including Penaeidins, lysozyme, crustins, Vibriopenaeicidae-induced cysteine and proline-rich peptides (VICPs), was significantly downregulated, while the expression of anti-lipopolysaccharide factors (ALFs) was upregulated. Moreover, LvIAP2 activated the promoters of the NF-κB pathway-controlled AMPs, such as shrimp Penaeidins and Drosophila drosomycin and attacin A, in Drosophila S2 cells. Taken together, these results reveal that LvIAP1 and LvIAP3 might participate in the host defense against WSSV infection, and LvIAP2 might be involved in the regulation of shrimp AMPs.
    PLoS ONE 08/2013; 8(8):e72592. DOI:10.1371/journal.pone.0072592 · 3.23 Impact Factor
Show more

Similar Publications