VIRAL CHARACTERISTICS
Equine infectious anemia virus is a lentivirus of the viral family retroviridae which infects equids. Retroviruses in general are single-stranded RNA, enveloped viruses which are obligate parasites that do not survive well in the environment. Through reverse transcription, RNA of the virus is transcribed to DNA and input into the genome of the cell it has invaded. From there the host cell will be controlled by the virus to produce the necessary proteins to help the virus replicate (Craigo et al. 2009). A human lentivirus that in some ways acts similar to EIAV is AIDS (North Carolina Department of Agriculture and Consumer Services undated) The virus is killed by boiling, sun UV rays, and most chemical disinfectants however its primary mode of transmission makes its weakness in the environment irrelevant (North Carolina Department of Agriculture and Consumer Services, undated) (see 'Transmission' for details).
Once EIAV has infected a horse the virus remains present through the clinical and subclinical phases of the disease, in other words the horse is infected for life. Clinical signs usually begin within 1 week to one month of infection initiating the acute infection which can in some cases be fatal (Payne et al. 2008). In chronic disease the horse is a carrier of the virus and periodic cases of viremia occur in which the horse shows clinical signs (Payne et al. 2008). The horse does NOT have to be immunosuppressed to become infected acutely or chronically by the virus. Virus replication occurs in the peripheral blood and tissue within macrophages (Payne et al. 2008). Though antibodies are produced against the virus they are non-protective antibodies and not the neutralizing antibodies required to specifically attack the virus (Hammond et al. 1997). Cell-mediated immunity is also present about a month after infection in the form of CD4+ and CD8+, cytotoxic T-cell activity (Hammond et al. 1997). This is thought to be the cause of recovery from the acute signs on EIAV viremia. By 6-8 months the immune system has matured enough to control most clinical outbreaks in the majority of patients (Hammond et al. 1997).
The cause for the virus’s ability to constantly evade the hosts immune defence mechanisms is in its capacity to replicate continuously and with high levels of variation. The virus evolves under the selective pressures of the hosts’ immune defence, and one genomic domain in particular, gp90 which encodes for envelope proteins. This is accomplished by amino acid deletion, insertion, and point mutations (Leroux et al. 2001). The immune system eventually recognizes and controls each new population; however some of the variations are able to escape inhibition and can lead to the periods of clinical disease (Leroux et al. 2001). This gets to the point where new “quasispecies” of virus population are formed with each episode of clinical disease in a chronically infected horse (Leroux et al. 2001). A study done on ponies infected with EIAV found that regardless of the number of episodes of clinical disease and viral replication rate, surprisingly similar levels of variation were found in the virus in each pony (Leroux et al. 2001). Thus the virus is able to persistently infect the animal via its changing viral envelope and evade recognition by host defenses. This is also the blockade to making vaccines for the virus as it is constantly changing therefore new ways to recognize the virus or alter host immune response are currently being researched.
Once EIAV has infected a horse the virus remains present through the clinical and subclinical phases of the disease, in other words the horse is infected for life. Clinical signs usually begin within 1 week to one month of infection initiating the acute infection which can in some cases be fatal (Payne et al. 2008). In chronic disease the horse is a carrier of the virus and periodic cases of viremia occur in which the horse shows clinical signs (Payne et al. 2008). The horse does NOT have to be immunosuppressed to become infected acutely or chronically by the virus. Virus replication occurs in the peripheral blood and tissue within macrophages (Payne et al. 2008). Though antibodies are produced against the virus they are non-protective antibodies and not the neutralizing antibodies required to specifically attack the virus (Hammond et al. 1997). Cell-mediated immunity is also present about a month after infection in the form of CD4+ and CD8+, cytotoxic T-cell activity (Hammond et al. 1997). This is thought to be the cause of recovery from the acute signs on EIAV viremia. By 6-8 months the immune system has matured enough to control most clinical outbreaks in the majority of patients (Hammond et al. 1997).
The cause for the virus’s ability to constantly evade the hosts immune defence mechanisms is in its capacity to replicate continuously and with high levels of variation. The virus evolves under the selective pressures of the hosts’ immune defence, and one genomic domain in particular, gp90 which encodes for envelope proteins. This is accomplished by amino acid deletion, insertion, and point mutations (Leroux et al. 2001). The immune system eventually recognizes and controls each new population; however some of the variations are able to escape inhibition and can lead to the periods of clinical disease (Leroux et al. 2001). This gets to the point where new “quasispecies” of virus population are formed with each episode of clinical disease in a chronically infected horse (Leroux et al. 2001). A study done on ponies infected with EIAV found that regardless of the number of episodes of clinical disease and viral replication rate, surprisingly similar levels of variation were found in the virus in each pony (Leroux et al. 2001). Thus the virus is able to persistently infect the animal via its changing viral envelope and evade recognition by host defenses. This is also the blockade to making vaccines for the virus as it is constantly changing therefore new ways to recognize the virus or alter host immune response are currently being researched.