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1、Antibody-Dependent Enhancement of Feline Infectious Peritonitis Virus Infection in Feline Alveolar Macrophages and Human Monocyte Cell Line U937 by Serum of Cats Experimentally or Naturally Infected with Feline Coronavirus Tsutomu HOHDATSU, Mika YAMADA, Ritsuko TOMINAGA, Kaori MAKINO, Kouji KIDA and
2、 Hiroyuki KOYAMA Department of Veterinary Infectious Diseases, School of Veterinary Medicine and Animal Sciences, Kitasato University, Towada, Aomori 034, Japan (Received 3 July 1997/Accepted 28 August 1997) ABSTRACT. Infection of the type II feline infectious peritonitis virus (FIPV) strain 791146
3、to primary feline alveolar macrophages and human monocyte cell line U937 was enhanced by the sera of cats experimentally infected with the 791146 strain, but not those of cats infected with KU-2 or UCD-1 strain of type I FIPV. The experiments using sera of cats with feline infectious peritonitis (FI
4、P) and of cats naturally infected with feline coronavirus (FCoV) revealed that infection of the FIPV 791146 strain to the U937 cells was enhanced only by the sera of cats infected with type II FIPV or feline enteric coronavirus. The samples positive for antibody-dependent enhancement (ADE) activity
5、had high neutralizing antibody titers against the FIPV 791146 strain and the samples negative for ADE activity had low neutralizing antibody titers. These findings support the previous results where a monoclonal antibody with neutralizing activity had high ADE activity, suggesting that there was a c
6、lose relationship between the neutralization and enhancement sites. And then it is also suggested that ADE of infection is likely to be induced by re-infection with the same serotype of virus in type II FIPV infection. Furthermore, U937 cells are considered useful and can be substituted for the feli
7、ne macrophages for determining ADE of FIPV-infection. KEY WORDS: antibody-dependent enhancement of infection, feline infectious peritonitis virus, feline macrophage, U937 cell. J. Vet. Med. Sci. 60(1): 4955, 1998 vaccination 1, 22, 2527, 30, 34. We previously reported that in vitro FIPV infection of
8、 feline alveolar macrophages is enhanced by murine monoclonal antibodies (MAbs) to the peplomer spike (S) protein of FIPV 10, 14. This antibody-dependent enhancement (ADE) activity by the MAb correlated with the neutralizing activity assayed by using CrFK 4, 10, 13, 21. Feline coronaviruses (FCoVs)
9、are divided into FIPV types I and II, and feline enteric coronavirus types I and II 23. The type II strains appeared to be more closely related to canine coronavirus (CCV) and transmissible gastroenteritis virus (TGEV), since immunodominant neutralization epitopes shared by the spike proteins of TGE
10、V, CCV, and the type II FCoV strains seemed to be absent in the type I strains 12. Recently, these findings were confirmed by sequence analysis. The sequences of spike genes of type II FCoVs have higher homologies with those of TGEV and CCV than those of type I isolates 18, 19. Dengue virus which ca
11、uses DHF/DSS has four serotypes differentiated by the neutralization test, and ADE of dengue virus infection often occurs in re-infection with a different serotype of the virus 6, 8, 9, 16, 17. However, the type of virus , re- infection by which will cause ADE at the highest frequency in FIPV infect
12、ion, is unclear. It has been reported that the frequency of type I FCoV infection is high in the field 11. In the present study, ADE of infection with the type II FIPV strain 791146 was examined with sera of cats experimentally infected with FIPV and naturally infected with FCoV. Monocytic cells use
13、d for determination of the ADE activity were feline alveolar or peritoneal Feline infectious peritonitis (FIP) is a virus-induced chronically progressive and usually fatal disease in domestic and wild Felidae. The causative agent of this disease is FIP virus (FIPV) which belongs to the family Corona
14、viridae. The natural route of FIPV infection is unknown although cats can be experimentally infected by oral, nasal, and parenteral administration of the virus. Following infection by these routes, FIPV first replicates in the epithelial cells of the upper respiratory tract and intestine 31. Clinica
15、lly apparent FIP occurs after the viruses infect macrophages and monocytes, and then cross the mucosal barrier and spread throughout the body of the cat. Generally, macrophages play an important role in non-specific defense against viral infection. However, it is also known that some viruses bound t
16、o antibodies invade macrophages via the Fc region of the antibody and the Fc gamma receptor (Fc g R) of the macrophage, and eventually the antibody leads to the enhancement of infection 2, 69, 15, 28, 29, 32. The disease caused by this infection mechanism is dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). The antibody against FIPV is also known to enhance the FIPV infection and accelerate the disease onset in cats 24, 26, 33. Following experimental FIPV infection, cats with FIPV-neu
