Feline leukemia virus strain FRA
Species:
Gammaretrovirus, Orthoretrovirinae, Retroviridae
Description and Significance:
Feline leukemia virus (FeLV) is a retrovirus. It is named a retrovirus because of the way it behaves within infected cells. Feline leukemia virus and all other retroviruses produce an enzyme called reverse transcriptase. The retrovirus is able to insert copies of its genetic material into cells in which they would like to infect. Feline Leukemia Virus is circular in shape and consists of an envelope, a nucleocapsid, and a nucleiod. The virus capsid is enveloped. The virions are spherical to pleomorphic. They measure 80-100 nm in diameter. The virions have surface projections which are densely dispersed. There are small distinctive glycoprotein spikes that evenly cover the surface of the virion. FeLV is made up of genomic nucleic acid. It is single stranded RNA and it is made up of ssRNA.
This infection effects felines. Feline Leukemia Virus is not very common in the United States. The prevalence of the infection varies immensely depending on the health, age, environment, and lifestyle of the cat. Approximately 2 to 3% of all cats are infected with this rare disease. However rates rise significantly depending on if the cats live outdoors, their immune system is not good, their very young, or if they are in contact with other cats who already have the virus. (Source: ICTVdB)
Three types of FeLV:
There are three horizontally transmitted FeLV subgroups: FeLV subgroup A (FeLV-A), FeLV-B, and FeLV-C. These have been defined by viral interference assays which detect genetic sequence variation in the viral surface glycoprotein of the envelope gene. FeLV-A is an ecotropic virus which is transmitted in nature. FeLV-B is a polytropic virus that is found in conjunction with FeLV-A and is due to recombination or mutations. FeLV-C, is also a polytropic virus is not as common than the other two types but is found in conjunction with FeLV-A or FeLV-A and FeLV-B. This third type tends to be fatal because it produces aplastic anemia. FeLV-C also is due to recombination or mutations.(Source: Chen, H and Phipps, A)
Genome structure:
The genome of the Feline Leukemia Virus is dimeric, unsegmented and contains a ssRNA. The genome is -RT and a positive-sense, single-stranded RNA. Minor species of genomic nucleic acid are also found in virions. The encapsidated nucleic acid is mainly of genomic origin but virions may also contain nucleic acid of host origin, including host RNA and fragments of host DNA believed to be incidental inclusions. The complete genome of one monomer is 7,000-11,000 nucleotides long. The 5'-end of the genome has a methylated nucleotide cap with a cap sequence type 1 m7G5ppp5'GmpNp. The 3'-terminus of each monomer has a poly (A) tract and the terminus has a tRNA-like structure.(source ICTVdB)
Ecology:
The FeLV virus needs a host to survive on which is why the virus cannot survive out of the body for usually more than eight hours. Hence, they have little effect to the environment.
Pathology:
Transmission of feline leukemia virus is through contact with saliva, nasal secretions, urine, feces, and milk from infected cats. The transfer of virus occurs when a cat is bitten, during mutual grooming or when cats use the same litter lox or feeding dishes. Transmission can occur through milk when an infected mother cat breast feeds her kittens. Or, it can even be transfered before the kittens are born. However kittens have the ability for their immune system to fight this virus if it is in the early stages.
Glycoproteins that protrude from the gammaretrovirus membrane mediate entry into the cell during infection. The glycoproteins are trimers of heterodimers composed of surface and transmembrane subunits. The surface subunit contains an N-terminal domain that binds to receptor (6, 7, 15) and a C-terminal region that is disulfide bonded to the transmembrane subunit, which mediates fusion between the virus and cell membranes.(source: Barnett et al).
What occurs in the Cell Once Infected:
Once a cell becomes infected, recombination of the viruses occur at preferred locations within the virus. Homologous recombination between sequences of marked purine-pryimidine strand bias at 3' junctions usually follows or occurs within the sequence ACCCC at 5' junctions. Some recombination sites also resemble recombinase recognition sequences utilized in immunoglobulin, and T-cell receptor variable-region joining. (Source: ICTVdB)
Application to Biotechnology
Due to the nature of the Feline Leukemia Virus, it is difficult to cultivate the virus or grow them into large quantities because the virus does not survive very long out of the felines body. Most of the researches have to collect the sample from infected felines instead of grown cultures. However, scientists have been able to produce monoclonal antibodies using mice, which helps destroy the virus in its tracks. The buffer that is used is PBS of a pH of 7.2., and is made up of a 0.05% sodium azide. This anti-FeLV monoclonal antibody is prepared in tissue culture and then the antibody is purified using Protein A affinity chromatography. The purified monoclonal antibody is of the IgG1 Kappa class and is able to recognize p27 antigen precursor and higher molecular weight precursors containing this antigen. Scientists producing this monoclonal antibody have produced good results in ELISA and Western Blots.( Source: Immunology consultants Laboratory)
Differential Pathogenicity of Two Feline Leukemia Virus Subgroup A Molecular Clones, pFRA and pF6A Study:
In this article it was stated that recent studies with neonatal cats, were inoculated with plasmid DNA containing a clone of FeLV derived from the Rickard strain of FeLV-A (pFRA). The cats inoculated with pFRA strain developed the classic FeLV infection with the secondary viremia. Four out of five animals showed enhanced tumor growth in a period of 28 to 55 weeks after they became infected. The fifth cat underwent a subgroup A-to-A/B-to-A/B/C transition and developed anemia at 65 weeks. Therefore genetic evidence of recombination between exogenous FeLV and endogenous FeLV-like viruses was detected in the first few weeks following infection. However, FeLV-B was rarely detected in the terminal tissues and if it was it was usually found at 30 to 78 weeks after infection. It was also not detected in the plasma from three out of seven secondary viremic cats whom were infected with FeLV-b or FeLV-C. This observation suggested that strain FRA was more recombinogenic and more virulent than other FeLV-A isolates or that the DNA, or the route of challenge enhanced recombination and the pathogenic process. (Source: Phipps, 2000)
References
Barnett et al, 2003, Structure and Mechanism of a Coreceptor for Infection by a Pathogenic Feline Retrovirus, Journal of Virology, V.77, 2717-2729.
Chen, H, 1998, Pathogenicity Induced by Feline Leukemia Virus, Rickard Strain, Subgroup A Plasmid DNA(pFRA), Journal of Virology, V.72(9): 7048–7056.
Immunology consultants Laboratory.http://www.icllab.com/ccp1225-monoclonal-anti-feline-leukemia-virus-p27-mflv-20m-8d11.htm
ICTVdB - The Universal Virus Database, version 4. http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/
Phipps, A, 2000, Differential Pathogenicity of Two Feline Leukemia Virus Subgroup A Molecular Clones, pFRA and pF6A, Journal of Virology, V. 74(13): 5796–5801.
