Method of propagating chicken infectious anemia virus

Details Method of propagating chicken infectious anemia virus Method of propagating chicken infectious anemia virus

2000-03-10

2003-07-15

Salimi, Ali R. (Department: 1648)

Chemistry: molecular biology and microbiology

Animal cell, per se ; composition thereof; process of...

C435S005000, C435S235100, C435S236000, C435S239000

Reexamination Certificate

active

06593134

ABSTRACT:

FIELD OF THE INVENTION
The present invention relates to methods for isolating, identifying, quantifying, and propagating chicken infectious anemia virus, in particular, for vaccine production.
BACKGROUND OF THE INVENTION
Chicken infectious anemia virus (CIAV), also known as chicken anemia virus (CAV) or chicken anemia agent (CAA), belongs to the group of Circoviridae. CIAV was first isolated in Japan in 1979 during an investigation of a Marek's disease vaccination break (Yuasa et al.,
Avian Dis
. 23:366-385 (1979)). Since that time, CIAV has been detected in commercial poultry in all major poultry producing countries (von Bülow et al., in
Diseases of Poultry
, 10
th
edition, Iowa State University Press, pp. 739-756 (1997)).
CIAV can cause clinical disease, characterized by anemia, hemorrhages and immunosuppression, in young susceptible chickens. Atrophy of the thymus and of the bone marrow are characteristic and consistent lesions of CIAV-infected chickens. Lymphocyte depletion in the thymus, and occasionally in the bursa of Fabricius, results in immunosuppression and increased susceptibility to secondary viral, bacterial, or fungal infections which then complicate the course of the disease. Infection of young chicks (less than 3 weeks) causes anemia, immunosuppression, morbidity and sometimes mortality if the chicks are free of maternal antibodies against CIAV. In chickens with maternal antibodies virus replication is suppressed until the antibodies disappear at approximately 3 weeks of age. After 3 weeks of age, infection is mostly subclinical but may cause changes in production of cytokines affecting the development of optimal immune responses to natural infections and vaccinations. The immunosuppression may cause aggravated disease after infection with one or more of Marek's disease virus (MDV), infectious bursal disease virus, reticuloendotheliosis virus, adenovirus, or reovirus. It has been reported that pathogenicity of MDV is enhanced by CIAV (deBoer et al., In
Proceedings of the
38
th
Western Poultry Diseases Conference
, p. 28, Tempe, Ariz. (1989)). Further, it has been reported that CIAV aggravates the signs of infectious bursal disease (Rosenberger et al.,
Avian Dis
. 33:707-713 (1989)). Additionally, subclinical CIAV infection in older chickens is correlated with decreased performance in broiler flocks (McNulty et al.,
Avian Dis
. 35:263-268 (1991)). CIAV is highly resistant to environmental inactivation and some common disinfectants, characteristics that may potentiate disease transmission. The economic impact of CIAV infection on the poultry industry is reflected by mortality of 10% to 30% in disease outbreaks, a possible role in vaccine failures, and lower performance of infected flocks due to subclinical infection.
CIAV is a small, non-enveloped icosahedral virus of 25 nm diameter, and contains a genome consisting of 2.3 kb circular, single-stranded DNA. Two polypeptides have been detected in purified virus preparations; a major polypeptide of about 50 kilodaltons (kDa) termed VP1, and a 24 kDa polypeptide termed VP2. These two polypeptides together form a major epitope for the production of virus-neutralizing antibodies. Genomic DNA sequences of several different isolates of CIAV have been reported. Isolate Cux-1 was sequenced by Noteborn et al. (Noteborn et al.,
J. Virol
. 65:3131-3139 (1991)) revealing 3 open reading frames (ORFs) that potentially encode polypeptides of 51.6 kDa, 24.0 kDa, and 13.6 kDa. As positioned in the genome, the three ORFs either partially or completely overlap one another. There was only one promoter-enhancer region upstream of the ORFs, and a single polyadenylation signal downstream of the ORFs. A single unspliced mRNA of 2100 bases is transcribed from the Cux-1 genome (Noteborn et al.,
Gene
118:267-271 (1992)). Another group also sequenced the Cux-1 strain; however, differences were noted between their sequence data and those from Noteborn et al. (Mechan et al.,
Arch. Virol
. 124:301-319 (1992)). The nucleotide sequence of strain 26P4, isolated in the U.S.A., also showed a number of nucleotide differences when compared with sequences of Cux-1 (Claessens et al.,
J. Gen. Virol
. 72:2003-2006 (1991)). Despite the differences in nucleotide sequences found in various isolates from around the world, only minor differences in amino acid sequences have been noted. For these reasons, it has been assumed that CIAV is a highly conserved virus.
Presently, the process by which CIAV causes chicken infectious anemia is poorly understood. When strain CIA-1 is introduced into susceptible 1-day old chicks, CIA-1 produces signs and lesions characteristic of chicken infectious anemia including low hematocrit values, depletion of erythrocytes and lymphoid cells in the bone marrow, depletion of lymphoid cells of the medulla and the cortex of the thymus (herein referred as T-cells), and inflammatory changes in the liver, heart and kidney (Lucio et al.,
Avian Dis
. 34:146-153 (1990)). One or more of the polypeptides encoded by the CIAV ORFs may play a role in the pathogenesis of chicken infectious anemia by facilitating invasion into susceptible cells, and/or initiating T-cell apoptosis.
Exposing hens to CIAV may induce maternal antibody in chickens which may help protect against CIAV infections in their progeny. However, such vaccination with any of the CIAV strains has inherent problems including the potential of vertical (through the egg) transmission, and contamination of the environment. It is therefore desirable to develop a vaccine having as the immunogen a purified polypeptide(s) associated with CIAV.
When CIAV was first isolated in 1979, (Yuasa et al., “Isolation and Some Characteristics of an Agent Inducing Anemia in Chicks,”
Avian Dis
. 23:366-385 (1979)), the only method of propagation was by chick inoculation. The Gifu strain of CIAV was subsequently found by Yuasa et al. (Yuasa, “Propagation and Infectivity Titration of the Gifu-1 Strain of Chicken Anemia Agent in a Cell Line (MDCC-MSB1) Derived From Marek's Disease Lymphoma,”
Nat. Inst. Anim. Health Q
. 23:13-20 (1983)) to replicate in two lymphoblastoid cell lines, Marek's disease cell culture (MDCC)-MSB1 (MSB1) (Akiyama et al., “Two Cell Lines From Lymphomas of Marek's Disease,”
Biken J
. 17:105-116 (1974)), and MDCC-JP2 (Yamaguchi et al., “Establishment of Marek's Disease Lymphoblastoid Cell Lines from Chickens with BABK of B Blood Groups,”
Biken J
. 22:35-40 (1979)), and the lymphoblastoid avian leukosis virus-transformed cell line, LSCC-1104X5 (Hihara et al., “Establishment of Tumor Cell Lines Cultured From Chickens With Avian Lymphoid Leukosis,”
Nat. Inst. Anim. Health Q
. 14:163-173 (1974)). Two other Marek's disease cell lines, MDCC-RP1 (Nazerian et al., “A Nonproducer T Lymphoblastoid Cell Line From Marek's Disease Transplantable Tumor (JMV),”
Avian Dis
. 21:69-76 (1977)) and MDCC-BP1 (Yuasa, “Propagation and Infectivity Titration of the Gifu-1 Strain of Chicken Anemia Agent in a Cell Line (MDCC-MSB1) Derived From Marek's Disease Lymphoma,”
Nat. Inst. Anim. Health Q
. 23:13-20 (1983)), and one lymphoid leukosis line, LSCC-TLT-1 (current terminology: LSCC-CU 10) (Calnek et al., “Establishment of Marek's Disease Lymphoblastoid Cell Lines From Transplantable Versus Primary Lymphomas,”
Int. J. Cancer
21:100-197 (1978)) apparently failed to support the growth of the virus. More recent reports (Chandratilleke et al., “Characterization of Proteins of Chicken Infectious Anemia Virus with Monoclonal Antibodies,”
Avian Dis
. 35:854-862 (1991) and Renshaw et al., “A Hypervariable Region in VP1 of Chicken Infectious Anemia Virus Mediates Rate of Spread and Cell Tropism in Tissue Culture,”
J. Virology
70:8872-8878 (1996)) suggest that other MD cell lines such as MDCC-CU22 (Calnek et al., “Spontaneous and Induced Herpesvirus Genome Expression in Marek's Disease Tumor Cell Lines,”
Infect. Immun
. 34:483-491 (1981)) and a reticuloendotheliosis virus-transformed T-cell line, RECC-CU205 (Schat et al, “Stable Transfec

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