Mouse Anti-FPV monoclonal antibody, clone IN963

Feline parvovirus disease (FP), also known as feline panleukopenia, feline plague, and feline infectious enteritis, is an acute, highly contagious disease caused by feline parvovirus (FPV). Cats under 1 year old are most susceptible to infection, especially kittens aged 3 to 6 months. Sick cats mainly show a sharp decrease in the number of white blood cells in the body. FPV also causes great damage to the digestive system of cats, and sick cats show severe digestive symptoms. FP has been defined as one of the most serious infectious diseases for cats in many countries in Europe and America. FPV is a single-stranded DNA virus that can replicate autonomously, with a genome length of about 5200bp. The size of FPV particles is about 20-24nm. Under an electron microscope, the virus particles are regular icosahedrons without capsules. The FPV genome has two open reading frames, one is the non-structural proteins NS1 and NS2, and the other is the structural viral proteins VP1 and VP2. The non-structural protein of FPV is encoded by the NS gene and is mainly formed in the early stage of virus invasion, so it is called replication protein. NS1 protein plays an important role in DNA replication, regulation of DNA damage response and apoptosis pathways, and is essential for the successful completion of the viral infection cycle and the promotion of pathology. NS2 protein consists of 657 amino acids, which is involved in regulating the nucleocytoplasmic transport and post-translational modification of NS1, thereby affecting the replication and transport of FPV in the host and promoting the cytotoxic effect of NS1. The VP gene encodes the capsid protein that forms the capsid. The structural protein VP1 protein has 752 amino acids, and its extended N-terminus includes the domain required for cell entry. The structural protein VP2 has 584 amino acids and is the main capsid protein component, accounting for about 90% of the entire viral capsid. VP2 protein has an important epitope that stimulates the virus to produce neutralizing antibodies, and mutations at key amino acid sites of VP2 protein play a key role in the pathogenesis of viral infection. It can effectively stimulate the body to produce neutralizing antibodies and affect its pathogenicity, host range and hemagglutination. So far, VP2 protein has always been an important target protein for studying VLPs vaccines.

Figure 1. Parvovirus structures at low resolution. (Sources: Padron E, et al. 2005)

After FPV enters the animal body, there is usually an incubation period of about one week. Some animals will carry a small amount of virus for a long time, and the disease will occur when the external environment changes or a stress response occurs. Due to the influence of individual factors, external environmental factors, virus strain factors, etc., the clinical symptoms of sick cats are also varied, usually showing a biphasic fever, first rising to a high temperature of about 40°C, then the body temperature returns to normal, and then rises to a high temperature state after 1 to 2 days. In the early stage of the disease, there are usually symptoms of depression, loss of appetite, even complete insufficiency and diarrhea, followed by dehydration, persistent diarrhea and vomiting, followed by serious symptoms such as blood in the stool, vomiting blood, sunken eyes and lowered body temperature. At this time, a routine blood test will find that the number of white blood cells has dropped to below 2.0×10⁹/L (normal is 5.50×10⁹/L~19.50×10⁹/L), and the number of lymphocytes and neutrophils has decreased the most. Then the white blood cells will further decrease. When the number of white blood cells drops below 1.0×109/L, the mortality rate is close to 100%. The most acute cases often die suddenly without any symptoms, and are often suspected of death by poisoning. Pregnant cats often show symptoms of abortion because FPV can be vertically transmitted through the blood-fetal barrier. The appearance of the body of a cat infected with FPV is usually rough and messy, dull, sunken eyes, and dry subcutaneous tissue. The pathological changes in the autopsy are mainly in the digestive tract, manifested as gastrointestinal dilatation, intestinal mucosal congestion, bleeding, necrosis, and mesenteric edema. Exudation occurs in the jejunum and ileum, the intestinal villi become shorter or disappear, and the intestinal wall thickens. The mesenteric lymph nodes are enlarged, congested, bleeding, and even necrotic, showing a marble-like pattern. The changes in the liver, kidneys and other solid organs are not very obvious, but only congestion symptoms appear, and the spleen has pinpoint hemorrhages. The detection methods of FP include rapid test paper test, hemagglutination and hemagglutination inhibition (HA-HI) test, electron microscopy observation, immunofluorescence test paper test, real-time fluorescence PCR detection, etc. However, based on the convenience of operation and revenue status, the main clinical diagnosis methods include colloidal gold test paper test, immunofluorescence test paper test, real-time fluorescence PCR detection, etc.

Feline panleukopenia virus
Feline distemper virus
FPV virus