Inside the core of the virus are two copies of the single stranded RNA genome. After the equine is infected, the RNA undergoes reverse transcription (RT), meaning the enzyme is used to generate complementary DNA from the RNA template. This process then produces a double stranded DNA molecule that designates the provirus (Elsevier 2013). The proviral DNA of all EIA strands sequenced to date contains a prototypical retroviral genomic organization with the major genes gag, pol and env bounded at both ends (Issel 2012). Gag, pol, and env are the group antigens that form the viral core structure, RNA genome binding proteins, and are major proteins comprising the nucleoprotein core particle. Both gag and pol gene products are produced from a full-length viral messenger RNA (mRNA) while those encoded by env are translated from a single spliced mRNA species. The other proteins (Tat and Rev) are generated from mRNAs that have undergone many splicing …show more content…
The probability of infection is proportionally determined by the volume of blood on the mouthparts of the insects. Dear flies, horse flies, and in some cases stable flies are most likely the ones that will transmit the disease. Once transmitted, the virus is free inside the plasma or the cell associated and also in monocytes and macrophages (Timoney 2014). Many scientists believe that the disease is only blood borne, but all tissue and bodily fluids are potentially infected as well, especially in cases where the viral burden is high. Another common way that EIA is transmitted is through the use of unsterile surgical equipment, syringes, and needles or by the transfusion of infected blood. In rare cases mares can also transmit the disease if they have one or more clinical episodes. In Ireland a breakout of EIA occurred in an equine hospital due to the sharing of stalls for mares that were pregnant or having a foal. Sadly there is a very close relationship between just presence of the disease and severity of it which makes it hard for vets and scientists to determine the illness. Many of the clinical signs of EIA are results from the release of pro-inflammatory mediators of cytokines, especially tumor necrosis factor alpha, IL-1, IL-6, and the infection of macrophages (Timoney 2014). The suppression of platelet production mixed together with these