| Bovine immunodeficiency virus | |
|---|---|
Virus classification | |
| (unranked): | Virus |
| Realm: | Riboviria |
| Kingdom: | Pararnavirae |
| Phylum: | Artverviricota |
| Class: | Revtraviricetes |
| Order: | Ortervirales |
| Family: | Retroviridae |
| Genus: | Lentivirus |
| Species: | Lentivirus bovimdef |
Bovine immunodeficiency virus (BIV) is aretrovirus belonging to the genusLentivirus. It is similar to thehuman immunodeficiency virus (HIV) and infectscattle. The cells primarily infected arelymphocytes andmonocytes/macrophages.[1]
BIV was discovered in the late 1960s in the search for the infectious agent causing bovineleukemia/lymphosarcoma. This search led to the isolation and identification of three distinct classes of bovine retroviruses. BIV was specifically identified by Dr. Cameron Seger, a veterinarian of theLouisiana State University Agricultural Center, while he was studying dairy cattle at the Southeast Louisiana Experiment Station atFranklinton, Louisiana. The cows presented with high white blood cell counts, referred to as persistentlymphocytosis (PL) which is associated with the development of bovine leukemia/lymphosarcoma.[citation needed]
The first animal studied was an eight-year-oldHolstein cow (R-29), herwhite blood cell count was elevated and her physical condition was steadily declining; after delivering a calf she weakened and became severely emaciated. She had to beeuthanized andnecropsy was performed. The diagnosis was lymphosarcoma, however, none of the tumors usually associated with the diseases were present in the postmortem gross examination. Tissue samples were sent to Dr. Van Der Maaten at the National Animal Disease Center; Dr. Van Der Maaten was able to isolate the BIV.[citation needed]
When the isolated BIV was inoculated intocolostrum deprived young calves, they developed elevatedleukocyte counts. The lymphocytosis persisted for several months andlymphadenopathy was apparent in the subcutaneouslymph nodes. This was similar to cow R-29. These calves, however, did not decline as R-29 did, which led researchers to believe that the isolated BIV was not the causative agent of the bovine leukemia/lymphosarcoma. It was put into storage and went unstudied until the discovery thatacquired immunodeficiency syndrome (AIDS) was caused by HIV.[2]
One of the identifying characteristics of lentiviruses is being able to infect non-dividing cells. BIV, being a lentivirus has this characteristic.[3] BIV, like HIV, has two phases to its replication cycle. The first phase is theentry phase; it is initiated by high affinity of thevirus envelopeglycoprotein with a specific cell receptor. The attached virus enters the cell by one of two ways, receptor mediatedendocytosis or viral envelope-cellmembrane fusion. Once in the cell, the virus is uncoated and theRNA genome isreverse-transcribed intoDNA.[2] Some studies have found thatreverse transcriptase has a higher activity at low concentrations of Mn2+ ions when compared to Mg2+ ions; this finding is helpful in classifying the virus.[4] The DNA (provirus) is then transported into the nucleus where it integrates into the host cell genome. The second phase of thereplication cycle is virusexpression. During this phase theprovirus istranscribed. The transcript isspliced and the viral mRNA is transported to thecytoplasm where it is thentranslated. After translation, the viralstructural proteins assemble the virus particle at theplasma membrane and form a complex with the viral RNA as thevirus buds and is released from the cell. The virus matures afterproteolytic processing by the viralprotease (PR). The virus is then ready to infect another cell and repeat the process.[2]
The mature virus is about 110–130 nm in size, with thegenome being 8.4kb. The genome contains the usual retroviral structural genes including gag, pol, and env. These genes are surrounded by and 5’ and 3’ LTR. It also contains at least five non-structural accessory geneopen reading frames (ORF). These are in the region between the pol and env ORF. Other accessory genes include vif (viral infectivity factor), tat (transcription activator), and rev (protein expression regulator). In primate lentiviruses there is usually an ORF for nef (negative factor); this is not present in BIV. BIV has a structure like all retroviruses, and contains two copies of its positive sense single stranded RNA genome. It has two compartments: the envelope and the core. The envelope comes from the host cell plasma membrane, the virus takes the membrane as it buds and then inserts viral glycoproteins into its envelope. The core of the virus contains Gag and Gag-Polpolyproteins. These polyproteins are cleaved in the mature virus to their functional forms.[4]
As mentioned before, leukocytosis and lymphadenopathy are associated with early infection. Researchers do not know how long cow R-29 was infected with BIV so some of thepathogenesis is not known. Eventually thesymptoms resemble those of AIDS in humans.[3]
Like other retroviruses, BIV is spread through exchange ofbodily fluids. When looking at prevalence of BIV infection, it was found that BIV is more prevalent in the southern United States and most prevalent in South America.[5] When an animal tests positive, many of the animals within the herd are also positive. Some of the spread is attributed to reuse of contaminated needles used in vaccinations, communal sharing of colostrum by calves, and failure to completelysterilize instruments after invasive treatments.[2]