Research Progress on immunosuppressive principle of Porcine circovirus ⅱ infection

Circovirus infection is a newly discovered infectious disease. The infection rate of the disease to pigs is high, and it occurs widely all over the world, and it has become one of the infectious diseases that seriously affect the development of the industry. Circovirus mainly attacks the immune system of pigs, interferes with and destroys the production and maintenance of immune antibodies to diseases, resulting in a decline in resistance, which is easy to be secondary or complicated with other diseases. In recent years, scholars at home and abroad have done a lot of research on the mechanism of porcine circovirus invading the immune system. Some progress has been made in the replication mechanism of porcine circovirus, its effects on cytokines and lymphocytes, and its relationship with porcine dermatitis and nephrotic syndrome, which lays a foundation for the prevention and treatment of porcine circovirus infection.

At present, most scholars believe that porcine circovirus Ⅱ (Porcinecircovirus2,PCV-2) is the main cause of postweaning multisystemic weakness syndrome (Postweaningmultisystemicwastingsyndrome,PMWS). PMWS was first discovered in western Canada in the mid-1990s and has since been found in the United States, France, Germany, New Zealand, India, Korea, Japan and Hungary. At the end of 2001, PMWS occurred in some large-scale pig farms in southern China, and the epidemic broke out in 2002. At present, it has spread to almost all large-scale pig farms in China. A retrospective antibody survey of European archived sera showed that PCV-2 has been infected with pigs for at least 30 years, and PMWS has existed in pigs for at least 15 years, but no significant change in the genome of PCV-2 has been found in the past 10 years.

PCV-2 needs some other inducements or pathogens to promote the occurrence of PMWS and cause a wide range of clinical symptoms and pathological changes in infected pigs. For example, temperature factors (low temperature, high temperature), environmental factors (ammonia, endotoxin), stress factors (mixed groups of pigs, long-distance transport), immune stimulation (vaccines, adjuvants), pathogens (porcine reproductive and respiratory syndrome virus, pseudorabies virus, Haemophilus parasuis, streptococci, Pasteurella multocida and salmonella) co-infection [1]. Porcine PMWS associated with PCV-2 has occurred and prevalent all over the world, with a case fatality rate ranging from 10% to 30%. The death rate is as high as 40% in more serious areas, such as pig reproductive and respiratory syndrome (PRRS) positive pig farms. PCV-2 also has the characteristic of immunosuppression, which can make infected pigs unable to produce effective immune response to other pathogens, which is easy to be complicated by other pathogenic infections (such as mycoplasma, bacteria, viruses, parasites, etc.), which makes the diseases of large-scale pig farms more complicated. Because of the harm and economic loss caused by PCV-2 infection, the disease has been recognized by veterinarians and pig farmers all over the world as an important pig infectious disease after PRRS, and has become the focus of scholars all over the world. In particular, the study of the immunosuppressive effect of PCV-2 will be of great significance to explain the pathogenesis of PMWS, prevent and cure diseases in intensive pig farms and develop PCV-2 vaccine.

1 PCV-2 can infect mononuclear macrophages and dendritic cells, but does not replicate in them.

PCV-2 is a monocyte-macrophage virus. Although PCV-2 antigen and its nucleotides can be detected in the cytoplasm of antigen-presenting cells, even in lymphocytes, these cells are not targets for viral replication. MeehanBM et al. [2] observed the surface antigens of monocytes and monocytes-macrophages infected with PCV-2 by flow cytometry and found that there was no viral antigen on the surface of these immune cells infected with PCV-2. Comparing PCV-2 infected lymphocytes with PK-15 cells, the intermediate products of PCV-2 progeny virus and virus replication were found in PK-15 cells, but no analogues were found in lymphocytes. It is suggested that these lymphocytes are not the first target cells replicated by PCV-2.

Dendritic cells (dendriticcell,DC) are the most powerful full-time antigen presenting cells (APC) in the body. Like other antigen-presenting cells, DC can significantly stimulate the proliferation of initial T cells (naiveTcell), while B cells and macrophages can only stimulate activated or memory T cells. Therefore, DC is the initiator of immune response in the body. Studies have shown that [3], 80% to 90% of the interaction between DC and PCV-2 occurs in the early stage of infection. Although no replication of PCV-2 was found in DC, the virus could persist in DC without losing its infectivity and causing DC death. Phagocytosis of PCV- 2 by DC did not induce changes in surface antigens such as MHC Ⅰ molecules, MHC Ⅱ molecules, CD80/80L, CD25 and so on. DC infected with PCV-2 does not re-infect homologous T lymphocytes, even if T cells have been activated. Co-culture of T lymphocytes and DC infected with PCV-2 did not cause PCV-2 replication and apoptosis of T lymphocytes and DC.

The mode of PCV-2 infecting DC not only evades host immunity, but also does not cause DC apoptosis. Because DC can migrate in the host and can be used as a means of transport to assist the movement of PCV-2 in the host, the depletion of lymphocytes in PMWS is not caused by the direct replication of the virus in lymphocytes, but should be involved in other factors.

Animals can still isolate the virus or detect viral DNA in various tissues on the 125th day after inoculation with PCV-2. This ability of persistence and continuous detoxification leads to the fact that even after the host recovers, the immune system still can not completely remove the virus, so it appears that PCV-2 is harmless to the immune system, but viral infection is directly related to clinical symptoms. ChangHW et al. [5] found that Gram-negative bacteria co-infection is an important factor to promote PCV-2 replication, at least play a certain role in the development of PMWS. Widespread infection of PCV-2 with DC and other antigen-presenting cells in lymphoid follicles is a major feature of PMWS, but the effect of PCV-2 on lymphocyte depletion and destruction of its function is not clear.

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