Investigations of Pro- and Anti-Apoptotic Factors Affecting African Swine Fever Virus Replication and Pathogenesis

نویسندگان

  • Linda K. Dixon
  • Pedro J. Sánchez-Cordón
  • Inmaculada Galindo
  • Covadonga Alonso
چکیده

African swine fever virus (ASFV) is a large DNA virus that replicates predominantly in the cell cytoplasm and is the only member of the Asfarviridae family. The virus causes an acute haemorrhagic fever, African swine fever (ASF), in domestic pigs and wild boar resulting in the death of most infected animals. Apoptosis is induced at an early stage during virus entry or uncoating. However, ASFV encodes anti-apoptotic proteins which facilitate production of progeny virions. These anti-apoptotic proteins include A179L, a Bcl-2 family member; A224L, an inhibitor of apoptosis proteins (IAP) family member; EP153R a C-type lectin; and DP71L. The latter acts by inhibiting activation of the stress activated pro-apoptotic pathways pro-apoptotic pathways. The mechanisms by which these proteins act is summarised. ASF disease is characterised by massive apoptosis of uninfected lymphocytes which reduces the effectiveness of the immune response, contributing to virus pathogenesis. Mechanisms by which this apoptosis is induced are discussed.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The pathogenesis of African swine fever in the resistant bushpig.

Bushpigs and warthogs are natural reservoir hosts of African swine fever virus (ASFV) in the wild, showing no clinical signs of disease when infected with the same highly virulent isolates of ASFV that induce rapid, haemorrhagic death in domestic pigs. In contrast to domestic pigs, infection of bushpigs with Malawi isolate results in low levels of virus replication and lymphocyte apoptosis with...

متن کامل

Development of a fluorescent ASFV strain that retains the ability to cause disease in swine

African swine fever is a contagious and often lethal disease for domestic pigs with a significant economic impact for the swine industry. The etiological agent, African swine fever virus (ASFV), is a highly structurally complex double stranded DNA virus. No effective vaccines or antiviral treatment are currently commercially available. We present here the development of a strain of ASFV that ha...

متن کامل

Requirement of cell nucleus for African swine fever virus replication in Vero cells.

The role of the cell nucleus in the development of African swine fever virus in Vero cells has been studied. No viral growth could be detected in enucleated cells under conditions that allow normal development of Sindbis virus. Furthermore, African swine fever virus DNA synthesis was inhibited more than 95% after infection of enucleated Vero cells as compared with normal cells.

متن کامل

African swine fever virus-cell interactions: from virus entry to cell survival.

Viruses have adapted to evolve complex and dynamic interactions with their host cell. The viral entry mechanism determines viral tropism and pathogenesis. The entry of African swine fever virus (ASFV) is dynamin-dependent and clathrin-mediated, but other pathways have been described such as macropinocytosis. During endocytosis, ASFV viral particles undergo disassembly in various compartments th...

متن کامل

African Swine Fever Virus: a new old enemy of Europe

African swine fever (ASF) is a highly contagious viral disease of swine with a mortality rate approaching 100 percent. African Swine Fever Virus (ASFV) is a double-stranded DNA virus with a complex molecular structure. Its large genome, encoding multiple virulence factors, allows for efficient replication, which takes place predominantly in the cytoplasm of monocytes and macrophages. Also, ASFV...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 9  شماره 

صفحات  -

تاریخ انتشار 2017