TEXTBOOK OF VETERINARY VIROLOGY

Prof. S. N. Sharma Dr. S. C. Adlakha

International Book Distributing Co.

TEXTBOOK OF VETERINARY VIROLOGY

Textbook of Veterinary Virology

Prof S N SharmaEx Professor of Virology Department of Veterinary Microbiology Punjab Agricultural University Ludhiana

Dr S C AdlakhaEx President National Academy of Veterinary Sciences New Delhi

International Book Distributing Co.(Publishing Division)

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PrefaceThis book is intended to fulfil the need of veterinary students in general and Post-Graduates in Microbiology in particular. besides the veterinary disease Investigators and Practitioners of veterinary medicine. Virology is one of those branches of science which has experienced a tremendous growth during the last few years especially in the area of Molecular Virology. The resultant information is spread over a number of publications. An attempt has been made to present all the relevant information in a concise manner including the latest advances. This book is divided into two parts: General Virology and Systematic Virology. There is plethora of literature on general virology, yet the authors have tried to present the basic principles of animal virology in a concise manner with the hope that the reader appreciates the nature of viruses, their pathogenicity. replication etc. In.the second part information on infections of vertebrates has been given with emphasis on the diagnostic and preventive aspects of virus infections of domestic animals and poultry. The organization of chapters is hierarchial and follows the taxonomy of animal viruses. A short family description precedes each chapter. To present the material in a limited number of pages, the authors have given only selected references at the end of each chapter. There are more viruses in domestic animals and birds than those discussed in this book; the viruses of little or no pathogenic importance or viruses encountered as contaminants in animal cell culture have been omitted. Greater importance has been given to viruses of economic importance in India and other developing countries of Asia and Africa. The authors will feel rewarded if this book will meet the requirements of the veterinary profession in the developing countries. The suggestions for improvement of this book in a future edition are welcome. Authors

ContentsAbbreviationsxi

PART IGeneral Virology1. Structure and Composition Classification of Viruses Viral Replication Cultivation of Viruses Viral Genetics Viral Pathogenesis 7. Persistent Infections 8. Viral Immunity 9. Epidemiology of Viral Diseases 10.. Viral Tumorogenesis 11. Viral Vaccines and Antiviral Agents 12. Diagnosis of Viral Diseases

2. 3. 4. 5. 6.

3 1334

46 55 65 76 81 87 94 102 115

PARTllSystematic Virology D.N.A. Viruses

13. PoxviridaeVaccinia Virus; Cow Pox Virus; Buffalo Pox Virus; Camel Pox Virus; Sheep Pox Virus; Goat Pox Virus; Lumpy Skin Disease; Ecthyma (Ort) Virus; Bovine Papular Stomatitis Virus; Milkers Node Virus; Swine Pox Virus; Myxoma Virus; Fibroma Virus; Fowl Pox Virus, 14. Parvoviridae Bovine Parvovirus; Porcine Parvovirus; Feline Parvovirus; Canine Parvoviruses.

129

150

\/iii

TeXlbook of Veterinary Virology15. Papovaviridae Bovine Papillomavirus type 1 and 2; Bovine Papilloma virus type-3; Bovine Papillomavirus type-4; Bovine Papillomavirus type-5; Bovine Papillomavirus type-6; Canine Papillomavirus; Rabbit Papillomavirus; Equine Papillomavirus. 16. Adenoviridae Bovine Adenoviruses; Ovine Adenovirses; Canine Adenoviruses; Infectious Canine Laryngotracheitis Virus; Equine Adenoviruses; Porcine Adeno-viruses; Avian Adenoviruses. 17. Hcrpesviridae Bovine Herpes Virus-I; Bovine Herpes Virus-2; Malignant Catarrhal Fever Virus; Bovine Herpes Virus-3; Hcrpes Virus of Sheep; Herpes Virus of Goats; Equine Herpes Viruses; Pseudorabies Virus; Simian Herpes Virus-I; Canine Herpes Virus; Fowl Hcrpes Virus-I; Duck Herpes Virus-I; Pigcon Hcrpes Virus; Marek's Disease Virus. 18. Unclassified DNA Virus African Swinc Fever Virus. RNA Viruses 19. Picomaviridae Apthovirus; Enterovirus; Swine Enteroviruses; Porcine Enterovirus-I; Porcine Enterovirus-9; Bovjne Enteroviruses; Avian Encephalomyelitis Virus; Duck Hepatitis Virus; Bovine Rhinovirus-I; Equine Rhinovirus 1 & 2. 20. Calciviridae Vesicular Exanthema Virus; Feline Calcivirus. 21. Togaviridae Alphavirus; Equine Encephalomyelitis Virus; Pestivirus; Bovine Viral Diarrhoea Virus; Border Disease Virus; Swine Fever Virus; Arterivirus; Equine Viral Arteritis. 22. Flaviviridae Japanese B Encephalitis Virus; Wesselsbom Virus; Louping III Virus. 211 159

164

176

206

231 234

247

COnlellls

23. Reoviridae Reovirus; Bovine Reovirus (type 1 & 3); Avian Reovirus type 1 to 5; Rotavirus; Bovine Rotavirus; Orbivirus; Blue Tongue Virus; AfricIDl Horse Sickness Virus. 24. Bimaviridae Infectious Bursal Disease Virus. 25. Coronaviridae Bovine Corona Virus; Canine Corona Virus; Feline Infectious Peritonitis Virus; Porcine Corona Viruses; Avian Infcctious Bronchitis Virus. 26. Orthomyxoviridae Equine Influenza Virus 1 and 2; Swine Influenza Virus; Avian Influenza Virus; Fowl Plague Virus. 27. Paramyxoviridae Paramyxoviruses; Avian Parnmyxoviruses; New Castle Disease Virus; Mammalian Parninfluenza Viruses; Parainfluenza-l; Parainfluenza-3 Virus in cattle; Parainfluenza-3 Virus in sheep; Parninfluenza-5; Morbillivirus; Canine Distemper Virus; Rinderpest Virus; Peste-DesPetits Virus; Pneumovirus; Bovine Respiratory Syncytial Vims. 28. Rhabdoviridae Vesicular Stomatitis Virus; Rabies Virus; Bovine Ephemeral Fever Virus; Marburg Vims. 29. Rettoviridae Oncoviruses; Bovine Leukaemia Virus; Feline Leukaemia Virus; Murine Leukaemia Viruses; Avian Leukosis Viruses; Avian Reticuloendotheliosis Viruses; Murine Mammary Tumour Virus; Bovine Syncytial Virus; Lentiviruses; Equine Infectious Anaemia Virus; Visna/Maedi Virus; Caprine Arthritis-Encephalitis Virus: Jaagsiekte (Ovine Pulmonary Adellomatosis Virus).

251

264 267

278

284

309

322

x

Textbook o/Velerinary Virology 30. Bunyaviridae Rift Valley Fever Virus; Akabane Virus; Nairobi Sheep Disease. 31. Toroviridae Breda Virus; Berne Virus. 32. Unclassified RNA Virus Borna Disease Virus. 33. Unclassified Agents Scrapie. Index 347

356 360 362 364

AbbreviationsAds adenoviruses avian encephalomyelitis virus agar gel immunodiffusion African horse sickness avian infectious bronchitis virus avian leukosis virus African swine fever virus bovine adenovirus border disease virus bovine ephemeral fever bovine herpesvirus bovine leukosis virus bovine papilloma virus bovine parvovirus bovine rhinovirus bluetongue virus bovine viral diarrhoea caprine arthritis-encephalitis virus chorio-allantoic membrane canine corona virus canine distemper virus contagious ecthyma complement fixation caprine herpesvirus counter immuno electrophoresis chicken kidney cell mediated immunity cytopathic effect canine parvovirus cytotoxic T cells

AEVAGID AHS

AIBV ALVASFV

BAV BDV BEV BHV BLV BPV BPoV BRVBTV

BVD CAEVCAM

CCV CDV CECF

CHVCIE

CKCM!

ere

CPE CPV

xiiCIL EAV EBV REV EHV EIAV ELISA EMF

Textbook of Veterinary Virology

FAV FCV FIPV FMD FPLVH

HAHI

IBD IBH IBR ICH IF IFN ILT IPIPV

mvJSRVKb

LD50 LCM MCF MDVMHV

MVV N

NIl'i1>V OAV PEV

cytotoxic T lymphocytes equine arteritis virus Epstein-Barr virus equine encephalomyelitis virus equine herpes virus equine infectious anaemia virus enzyme-linked immunosorbent assay electron microscope/microscopy fusion protein fowl adenovirus feline calcivirus feline infcctious peritonitis virus foot-and-mouth disease feline panleucopenia virus haemagglutinin haemaggl utination haemagglutination inhibition infectious bursal disease inclusion body hapatitis infectious bovine rhinotracheitis infectious canine hepatitis immunofluorescence interferon infectious laryngotracheitis immunoperoxidase infectious pustular vulvovaginitis Japanese encephalitis virus jaagsiekte retrovirus kilobases 50 percent lethal dose lymphocytic choriomeningitis malignant catarrhal fever Marek's disease virus major histocompatibility complex maedi-visna virus neuraminidase neutralization index Newcastle disease ovine adenovirus porcine enterovirus

Abbreviations

xiii

PI PPR PPV REV RIA RSV RVF SN SPY SV SVE TGE UV VE VN VSV

parainfluenza peste-des-petits-ruminants porcine parvovirus reticuloendotheliosis virus radioimmunoassay respiratory syncytial virus Rift valley fever serum neutralization sheep pox virus simian virus swine vesicular exanthema transmissible gastroenteritis ultraviolet vesicular exanthema virus neutralization vesicular stomatitis virus

PART!

GENERAL VIROLOGY

Chapter 1

Structure and

COlD position

The viral diseases of man and animals have been known for many centuries. The science of virology emerged during the last decade of last century. Ivanovski in 1892 reported that tobacco mosaic virus agent could pass through filters which retained bacteria. In 1898 Beijerinck showed that the tobacco mosaic disease agent differed fundamentally from toxin and it diffused through agar and he used the term 'contagium vivum fluidum' - that it was liquid or soluble. He also reported that only those plants which were growing and whose cells were dividing could be infected. The disease causing agent must be incorporated into the living protoplasm in order to propagate and it cannot multiply outside cells. Loeftler and Frosch in 1898 independently reported that foot and mouth disease of cattle could also be produced by a material passed through the filter which retained bacteria. Twort (1915) and d' Herelle (1917) recognised that bacteria also could be infected by filter passing agents. Virology is now recognised as a basic biological science and veterinary virology has grown immensely during the past few decades. The subject of virology is divided into four main divisions i) Animal viruses - the viruses of man and animals. ii) Insect viruses - the viruses of insects and worms. iii) Bacterial viruses (Bacteriophages). iv) Plant viruses - viruses of plants. The real nature of viruses has been elucidated since 1930. Stanley (1935) crystallized tobacco mosaic virus. Hershey and Chase (1952) discovered that only DNA of bacteriophage entered its bacterial host

4

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and only DNA was necessary for infection. Fraenkel-Conrat (1956) proved that RNA of tobacco mosaic virus carried all the information for growth. Since then an enormous upsurge in our knowledge regarding the nature of viruses and its molecular biology has taken place. Viruses have a very simple structure. The mature virus particle (Virion) consists of a central core of nucleic acid surrounded by protein coat. They vary in size ranging from 300 x 200nm of pox viruses to 20-25 nm of picornaviruses. Viruses can be distinguished from other unicellular microorganisms (Table 1.1). Lwoff and Toumier (1966) described the viruses having following five characters i) Possession of only onc type of nucleic acid, either DNA or RNA. ii) Reproduction solely from nucleic acid, whereas other agents grow from the sum of their constituents and reproduce by division. iii) Do not undergo binary fission. iv) Lack of genetic information for the synthesis of essential cellular systems. v) Use of ribosomes of their host cells.

Table 1.1IMPORTANf PROPERTIES OF UNICELLULAR ORGANISMS AND VIRUSES

Property

Bacteria Mycoplasma ChlamydiaDNA and RNA DNA and RNA DNA and RNA

Rickettsia VirusesDNA and Either DNA or RNA, not RNA both Some DNA and RNA viruses have infectious NA

1. Nucleicacid (NA)

2. Nucleicacid(NA) infectious

3. Ribol!omes + 4. Action of Nointerferon 5. Metabolic activity 6. Binary fission action

+No action

+Inhibifs growth

+No action Inhibits replication

+ +

+ +

+

++

Structure and Composition

5

The criteria given above clearly distinguish viruses from other microorganisms; the most important criterion is that viruses contain only one type of nucleic acid. DNA or RNA and are completely dependent on the host cell for their reproduction. Some viruses may persist in their host cells by integration of their genome (DNA) or DNA CQPy of their RNA into the genome of host cell. The viruses are not 'y virus neutralization test Control: The virus produces adequate immunity after natural infection. The inactivated vaccines do not give satisfactory immunity. A chicken embryo attenuated strains when administered subcutaneously, produce good immunity.Pigeon Herpesvirus It causes conjunctivitis: respiratory distress, diarrhoea, dehydration and emaciation with lesions in liver and other organs of pigeons. The virus grows in chicken embryo by CAM route and also in chicken embryo kidney and liver celJs. Pigeons 1-6 months of age are most often affected. Focal necrosis and A type intranuclear inclusions are found in the liver and kidneys. Marek's DiseaseViru~

(MDV)

It is a transmissible virus disease which mainly affects domestic fowl and is characterised by mononuclear infiltration around peripheral nerves and to lesser extent in skin, muscle, iris and internal organs. The disease affects mainly domestic poultry and is common in young birds of 2-5 months old. The first detailed account of the disease was published in Holland in 1914. The specific herpesvirus etiology was established in 1967. The disease occurs worldwide. In this country the disease was reported in 1970 and is prevalent in all parts of this country. Mohanty et al.(1973) reported annual losses to the tune of 40 million rupees to poultry industry of this country. Marek's disease is an important model for the study of tumorigenic potential of herpesviruses. Properties of the virus: Two types of virus particles, onc is naked virion measuring 35-100 nm and second type of virion particles are enveloped and measure 150-170 nm in size, have been described. The enveloped virion of MDV are of two types, one of which is found in the nucleus of infected cells and is 150-180 nm in diameter and presumed to be noninfectious. The second type found predominantly in cytoplasm and in feather follicle epithelial cells is infectious and measure 250-280. nm. The genome is double stranded DNA with a moleular weight of

Herpesviridae

199

lxlO' daltons. The G+C content is 46 percent. In cultured cells the virus is not readily demonstrated but preparations from lysed feather follicle epithelium reveal the presence of particles measuring between 275-400 nm in diameter. The virus survives for a long time at 60C in growth medium containing 10% calf serum and 7.5% dimethyl sulphoxide. All the strains isolated have been found to be antigenically homogenous but some differences have been reported. The virus cross reacts with herpes simplex, Aujeszky's disease virus, IBR and EpsteinBarr virus. The highly oncogenic MDV strains and their attenuated variants have been placed in one group and low o~cogenic or non oncogenic strains in second group based on immunodiffusion tests. The herpes virus of turkey (HVT) forms a third antigenically related group. There is certain DNA homology between HVT and MDV viruses. Cultivation: The virus can be cultivated in susceptible chickens, chicken embryos and cell cultures. When day old chicks are inoculated with suspected material the lesions can be detected after 2-4 weeks in ganglia, nerves and certain visceral organs. By fluorescent antibody technique many tissues of chicks show the viral antigens. The virus can also be cultivated on the CAM of susceptible chicken embryos or by yolk sac route. The virus produces discrete white pocks on the CAM. The virus grows in chicken kidney (CK) and duck embryo fibroblasts (DEF) and produces characteristic CPE in 6-14 days. The CPE consists of rounded and fusiform refractile cells and polykaryocytes which have inclusions in the nucleus. When cells from infected chicken kidney are grown, characteristic CPE is produced. The tumour, spleen, kidney, buffy coat or whole blood from affected birds is suitable material for virus isolation. Epidemiology: Most of the birds at the time of maturity have antibodies in MDY although the infection persists and virus is shed in the dander of feather follicles. Congenital infcction does not occur. The disease occurs most commonly in young birds between2-5 months of age. If the chickens are exposed on the day of hatching the disease develops at 3 weeks of age. Natural transmission is air borne through inhalation. The infectious virus is present in oral, nasal and tracheal secretions and in feather follicle epithelium. Genetic resistance, age and viral strains influence the outcome of infection. A small percentage of infected birds develop clinical MD. During rust few days of life, chicks are very susceptible to the virus. The virus matures in the feather

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collicle and is shed through desquamated cells into the environment. The infected feathers remains infected for 6 weeks or more. Blood or tumor material containing live, intact cells can transmit the disease. Infected whole cell cultures may transmit the disease but not cell free fluid as the virus is cell associated. Occasionally MD has also been reported from free flying birds like crow and myna. Pathogenesis: The outcome of infection of chickens by MDV is influenced by virus strain, route of infection, dose, age, sex, immune status and genetic susceptibility of the chickens. Subclinical infection with virus shedding is common. The infection is acquired by inhalation. The epithelial cells of respiratory tract are productively infected and contribute to cell associated viraemia involving macrophages. By sixth day there is productive infection of lymphoid cells in a variety of organs. During the second week after infection there is persistent cell associated viraemia followed by proliferation of T lymphoblastoid cells and after few days cells begin to die. The lesions result from infiltration and proliferation of T lymphocytes which may result in leukemia and inflammatory cell response to the lysis of nonlymphoid cells by the virus. Enlargement of one or more peripheral nerve trunks is one of the most constant gross pathological finding. The nerves are 3 times their normal diameter and show loss of striations, oedematous, grey or yellowish and somewhat translucent in appearance. The celiac, cranial, intercostal, mesentiric, brachial, sciatic and greater splanchnic nerves are mostly involved. The enlargement of the nerve is usually unilateral. Lymphoma-tous lesions affects the gonads, lungs, liver, spleen, kidney and thymus. The behaviour of MDV with lymphoid and non lymphoid cells differs considerably. In non lymphoid cells infectious virus particles are produced in feather follicle epithelium or non infectious virus particles or viral antigen is produced in other epithelial cells or in cell culture. In both cases the death of cell takes place. In lymphoid cells the transformation of cells take place with extensive proliferation without cell death. In these cells the presence of virus particles or the expression of viral antigen is not detected but in some Iymphoblastoid cell lines a low percentage of cells may produce viru~ particles or viral antigen. ~arek's disease is a progressive disease with variable signs. In neurolymphomatosis or classical disease there is paralysis of one or

Herpesviridae

201

both legs or wings. The early sign shown by the birds is incoordination. one leg held forward and other backwards. There is drooping of wings and lowering of head or neck. If vagus nerve is involved there may be dilation of crop and gasping. The acute marek's disease occurs in explosive outbreaks in large number of birds. The clinical signs are depression followed by ataxia and paralysis of some birds. In ocular lymphomatosis the iris of one or both eyes is gray in colour and the pupil is irregular ecentric. The cutaneous form of disease is recognised by nodular lesions upto 1 cm in diameter seen particularly at feather follicles. Immune reaction: The infected nonlymphoid cells contain viral antigens while infected lymphoid cells contain Marek's associated tumor specific antigen (MATSA). These antigens can be detected by immunofluorescence and immunodiffusion test. MATSA can be detected by using immune sera prepared from chickens or rabbits immunized with transplantable tumor cells or cultured lymphoblastoid cells but not by antiserum derived from chickens that have recovered from MD. MATSA has been associated with cells transformation. The birds develop both humoral and cell mediated immunity (CM!) after infection with MD. The virus specific antibodies appear 1-3 weeks after infection and persist throughout the life of bird. The presence of antibody does not have a significant protective effect but may decrease the severity of the disease. The resistance to MD is primarily due to CMI response. T cells probably play a double role in MD by providing target cells for transformation by MDV and also by participating in immune mechanism against the development of lymphoid tumors. MDV has an immunosuppressive effect. The progeny of infected birds acquire passive immunity which disappears within 3-4 weeks. Diagnosis: A tentative diagnosis is arrived at on the basis of symptoms and lesions. In classical form there is unilateral or bilateral paralysis of legs or wings, curling of toes, torticollis, dilatation of iris. In acute forms symptoms are rapid depression, emaciation and death. Most cases show oedematous swelling of vagus and sciatic nerves and of brachial, coeliac and lumber plexus. Detection of viral antigen by immunofluorescence is the reliable diagnostic procedure. MDV can be isolated by inoculation of susceptible chickens, cell cultures and embryonated chicken eggs. The specimens of choice are

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intact viable cens from buffy coat, spleen, tumour tissue or other lymphoid cens. Virus can also be isolated from skin and feather tips which contain cell free virus. The day old susceptible chicks ate inoculated intraperitoneally. After 18-21 days the birds show gross or microscopic lesions. The virus isolation and detection of serum antibody ftom the inoculated chickens should be undertaken. MDV produces characteristic CPE in duck embryo fibroblast (DEF) and chicken kidney (CK) cen culture. Characteristic plaques are produced in 6-14 days and consist of rounded refractile cells and polykaryocytes with cowdry type A inclusions. The virus produces pocks on the CAM of chicken embryos. Identification of virus isolated can be confirmed by immunofluorescent technique. The antibodies can be demonstrated in the sera of infected or recovered birds by agar gel precipitation test, indirect fluorescent antibody test or passive haemagglutination test. Control: MD is the first virus induced malignacy to be controlled by vaccination. There are three types of live vaccines available. These are herpes virus of turkeys (HVT). apathogenic strain of MDV and cell culture attenuated MDV. All these vaccines are equally effective. The vaccine virus persists in the vaccinated birds and does not prevent superinfection, replication or shedding of virulent MDV but prevents clinical disease. The resistance is life long in vaccinated birds. The mechanism of protection is due to cell mediated immunity response. The vaccinated chickens probably develop lymphopro1iferative lesions containing Marek's associated tumour specific surface antigen (MATS A) and a CMI response directed against MATSA protects the chickens against subsequent lymphoma formation by the ,:,irulent virus. The most extensively used vaccine is HVT. Chickens are generally vaccinated at hatching and should be reared in isolation. The hygienic procedures help to delay the exposure of the chickens and thus allow immunity to be established. ReferencesALLAN,

G.P.; YEARVAN, M.R.; TURllUEN, L.W.; BRYANS, J.J. and McCOLLUM, W.H., 1983. Molecular epizootologic studies of equifU! herpes virus-l infections by restriction endonuclease fingerprinting of viral DNA.American Journal of Veterinary Research. 44 (2): 263-27l.

BARAHONA,

H.; MELl!NDEZ, L.V. and MELNICK, J.L., 1974. A compendium of

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herpesviruses isolaJed from non human primates. Intervirology. 3: 175.

BAUDET, A.E.R.F., 1923. Mortality in ducks in the Netherlands caused by a fiIJrable virus fowl plaque. Tijdschi Diergeneesk. 50: 455-459. BUXTON, A. and FRASER, G., 1977. Animal Microbiology. Vo1.2. Blackwell Scientific Publications. Oxford. CAMPBELL, T.M. and STUDDERT, MJ., 1983. Equine herpesvirus type-1 (EHV1). Veterinary Bulletin53: 135-145. CHURCHll.L, A.E. and BlOGS, P.M., 1967. Agent on Marek's disease in tissue culture. Nature215: 528-30.DEWNETT~D.P.;

BARASA, 1.0. and JOOIINSON, R.H., 1976. Infectious bovine rhinotracheitis virus: studies on the veneral carrier status in range cattle. Research in Veterinary Scicnce20: 77-83.

DEv PRAKASII and RAJYA, B.S., 1970. Avian leucosis complex. I. Demographic studies. Il. Pathoanatomy and serum lactic dehydrogenase level of Marek's disease in natural infection. Indian Journal of AnimalSciencesAO: 282-296.

DEw, C. and McFERRAN, lB., 1966. Experimental studies on Aujesky's disease in cattle. Journal of comparative Pathology and Thcraeutics. 76: 379385. GmBS, E.P.J. and RWEYEMA.\iU, M.M., 1977. Bovine herpes viruses. Part. I. Bovine erpesvirus 1. Part 11. Bovine herpesviruses 2 and 3. Veterinary Bulletin, 47: 317-43 and 411-425. GREIG, A.S.; BAUMISTER, G.L.; MITCIIFLL, O. and BARKAR, C.A.V., 1985. Cultivation in tissue culture of an infectious agent from coital exantheme of cattle. A preliminary report. Canadian Journal of Comparative Medicine. 22: 119-122. GREWAL, GURDEV, SINOIl and SINGII, BALWANT, 1976. Incidence of Marek's disease virus infection in domestic fowl5 of Punjab (India). Avian Diseases. 20: 191-194. HANSEN, L.E., 1978. Laryngotracheitis. In M.S.Hofstad, B.W.Calnek, C.F. Helmboldt. V.M. Reid and H.W. Yoder, JR (Editors), Diseases of POUltry. Oxford a:ld IBH Publishing Co.New Delhi pp. 607-618.Infectiuous bovine rhinotracheitislinfectious pustular vulvovaginistis. 1984. Publication of Division of Pathology, Indian Veterinary Research Institute, Izatnagar, U.P.

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JAIN, N.C.; MANCHANDA, V.P.; GARO, D.N. and SHARMA, V.K., 1976. Isolation and characterisation of Equine herpes virus type-I. Veterinary Record.99: 57. JAIN, N.C.; SB1lJ, P. and PRASAD, G., 1986. Herpes virus infections. In National symposium on 'Current status of herpes virus infections in man and animals in India' held at at Department of Veterinary Microbiology, Haryana Agricultural University, Hisar. KAHRS, R.F., 1985. Viral disease of cattle. Kalyani Publishers, Ludiana. HAY, H.G. and TITI'SLER, R.P., 1925. Tracheolaryngitis in Poultry. Journal of of American Veterinry Medical Association. 67: 229-23l. MEHROTRA, M.L.; RAJYA, B.S. and KUMAR, S., 1976. Infectous Bovine rhinotracheitis (IBR). Keratoconjuctivitis in calves. Indian fournal of Veterinary Pathology. 1: 70-73. MEHROTRA, M.L.; KUMAR, S. and RAJYA, B.S., 1981. Note on passive of infectious haemagglutination test for detection bovinerhinotracheitis infectious pustular vulvovaginitis (lBRIPN) virus antibody. Indian Journal of Animal Scineces. 51: 559-569. Mll.LER, NJ., 1955. Infectious necrotic rhinotracheitiS of cattle. Journal of American Veterinary Medical Association. 126: 463-467. MOHANTY,. G.C.; AcHARJYo, L.N. and RAJYA, B.S., 1973. Epidemiology of Marek's disease (MD). Stuides on the incidence of M.D. precipitins in some zoo birds. Poultry Scinece 52: 963-966 MOHANTY, S.B., 1990. Pseudorabies virus. In virus infections of ruminants edited by Z. Dinter and B. Morein. EIsevier Science Publishers B.V. Amsterdam. MOHANTY, S.B. and DUTIA, S.K., 1981. Veterinary Virology. Lea and Febiger, Philitdelophia. MUKERJI, A.; DAS, M.S.; GHOSH, B.B. and GANGULY, lL., 1963. Duck plague in West Bengal I and /I. Indian Veterinary Journal. 40: 457-462. NAZARIAN. K.; LINDEHL, T.; KLElN, G. and LEE, L.F., 1973. Deoxyribonucleic acid of MareKs disease virus in virus induced tumors. Journal of Virology. 12: 341-346. PARIHAR, N;S.; RAJYA, B.S. and Gll.L, B.S., 1975. Occurrence of malignant catarrhalfever in India. Indian Veterinary Journal. 52: 857-859. PLOWRIGHT, W., 1990. Malignant catarrhal fever virus. In virus Infections of

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ruminants, edited by D. Zinter and B. Morein. Elsevier science Publishers, B.V. Amsterdam.PuRCHASE,

H.G., 1972. Recent advances in thl: knowledge of Marek's disease. in veterinary Science and comparative Medicine. 16: 22953.Advan~es

SAMBY AL, D.S. and BAXI, K.K., 1979. Isolation of Marek's disease virus from tissues of birds suspected for Marek's disease. Poultry Advisor, 12: 17-19. SHARMA, G.L.; LALL, IM and BHALLA, N.P., 1965. Histopathological evidence of equine viral abortion in India. Indian Journal of Veterinary Science and Animal Husbandry 35: 18-23. Singh, G.; Singh, B.; Guta; P.P. and Hothi, D.S., 1979. Epizootiological observations on malignant catarrhal fever and transmission of the disease in buffalo calves. (BubaIus bubalis). Acta Veterinaria Bruno. 48: 95-103. SINGH, S.B.; SINGH, G.R. and SINGH, C.M., 1964. A preliminary report on the occurrence of infectious laryngotracheitis in poultry in Punjab. Poultry Science. 43: 492-494. SlRAUB, P.C., 1990. Infectious bovine rhinotracheitis virus. In virus infections of ruminants, edited by D. Zinter and B. Morein. Elsevier Science Publishers B.V. AmsterdaIJ).. STUDENT, M.I; SIMPSON, T. and Rozilllian, B., 1981. Differentiation of respiratory and abortigenic isolates of equine herpes virus I by restriction endonucleases. Science. 214: 562. WrITHMAN, G.; GASKELL, R.M. and RZIHA, H.J., 1984. Latent herpes virus infections in Veterinary Medicine. In a seminar in the commission of European Communities held at Tubingen. FRG. Martinus, Nijhoff Publishers, Boston.

Chapter 18

Unclassified DNA virusAfrican swine fever Virus (ASFV) The African swine fever virus which was previously included in family Iridoviridae has now been taken out of this family but not yet been placed under any other family. African swine fever virus produces highly contagious fatal disease in pigs with some similarities to swine fever. The disease causes serious economic losses and is indigenous to African continent. The disease first appeared in 1910 in East Africa and Africa and then it spread to other territories of the continent. ASF was reported in 1957 from Portugal. A number of isolated outbreaks have been reported from Spain, France and Italy. In 1971 the disease was reported from Cuba. The disease has not been reported to exist in this country. Property of virus: The virus particle measures 200-220 nm in diameter and consists of electron dense centrally placed nucleoid surrounded by a hexagonal outer shell. The virion acquires an additional outer envelope from plasma membrane. The genome consists of single stranded DNA, which codes for about 25 structural proteins and also some non structural proteins. The nucleoprotein core is surrounded by icosahedral sheet and contains 9% phospholipid. The virus is stable at room temperature for severn I weeks. The virus is inactivated in 30 minutes at 56 C and survives for months and even years in refrigerated meat. The virus survives in chilled carcases for 15 weeks or longer and upto 6 months ID processed meat. The virus is stable over a wide pH range and is inactivated quickly in 2% NaOH.

Unclassified DNA Virus

207

The virus is not inactivated by crystal violet which is used to inactivate swine fever virus. The virus does not possess the property of haemagglutination but infected leucocyte cultures haem adsorb pig rbe. The haemadsorption is inhibited by African Swine fever serum. Different strains do not cross protect and it is probable that several anti genic types exist The virus was fIrst propagated in the yolk sac of chicken embryos. Most of the strains replicate in the buffy coat cells of swine bone marrow. The virus produces syncytia and nuclear and cytoplasmic inclusions. in infected syncytia and nuclear and cytoplasmic inclusions in infected cell culture. however some strains do not produce CPE. Epidemiology: Recovered animals develop long resistance to reinfection with homologous virus type but not against heterologous types. The virus from the infected animals is excreted in secretions and transmit the virus by contact or by aerosol route. The wart hogs in Africa act as reservoirs and transmit the infection to domestic pigs by indirect contact. The surviving pigs act as life long carriers. lice and ticks of pigs transmit the infection. Since the virus is resistant to atmospheric conditions and persists in the tissues of the carcases of carrier animals. the feeding of swill containing uncooked pork scraps is responsible for secondary epidemics and virus outbreaks. The outbreak in Portugal. Brazil etc. were due to feeding of untreated swill. The swine fever vaccine is also responsible for spread of outbreaks. In Brazil swine fever vaccine was contaminated with ASFV. In the inactivated crystal violet swine fever vaccine. the virus of ASFV survived and caused outbreaks. Diagnosis: African swine fever is suspected when there is acute or paracute haemorrhagic disease with high mortality is encountered in SF vaccinated pigs. The provisional diagnosis can be made on clinical and postmortem lesions. A confirmation can be made by inoculating pigs susceptible and immune to ASF with the suspected material. The virus isolation can be attempted in cell culture from blood. splcen lymph nodes of infected animals. The infected leucocyte cultures haemadsorb pigs rbe and this property is not shown by SFV. The test based on this property of ASFV is applied for diagnosis. Complement fixation and gel diffusion tests are applied for detection of ASFV antibodies. Fluorescent antibody is also useful in the diagnosis. Contrpl: Vaccination with killed as well as with live virus has not

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been effective. The virus appears to be a poor antigen. Pigs recovered from the disease are immune to homologous strain but not heterologous strains. The effective method of eradication is by slaughter and strict import regulations for meat products as well as live animals.ReferenceCOOGlNS, L., 1974. African swine fever virus. Pathogenesis: Progress in medical Virology. 18: 48-63. DETRAY, D.E., 1964. African swine fever virus. Advances in Veterinary Science 8: 299-333MALlNQUlST,

W.A. and HAY, D., 1960. Haemodsorption and cytopathic effect produced by African Swine fever virus in swine bone marrow and buffy coat cultures. American Journal of Veterinary Research 21, 104-108.

MAINER, F.D., 1975. African swine fever. In Diseases of swine, 4th Edition, Edited by H.W.Dunne and A.D. Lemann, Iowa, Iowa State University, Ames, Iowa. RuSSELL, P.H. and EDlNGTON, N., 1985. Veterinary viruses. The Burlington Pr~ss (Cambirdge) Ltd. Foxton, Cambridge

PARTII

SYSTEMATIC VIROLOGY R.N.A. VIRUSES

Chapter 19

Picornaviridae

Picorna name was introduced in 1962 to describe a group of very small RNA viruses. The family contains four genera namely Enterovirus, Rhinovirus, Cardiovirus and Aplhovirus. The viruses included in this family are small icosahedral nonenvcloped measuring 22-30 nm in diameter. The capsid appears smooth and round in outline and made up to 60 capsomeres each consisting of onc molecule of each of the four major polypeptides: VPl, 2,3 each of about 30K and VP4 of about 1OK. The picorna virus capsid contains one moleucle of infectious single stranded RNA of positive polarity with a molecular weight of about 2.5 x 1()6. A convalentIy linked protein VPg is present at 5' terminus of the RNA. Four major polypeptides participate in the construction of the capsid. Purified VPl elicit neutralising antibody, though less immunogenic than intact inactivated virus particle. This discovery has provided a major impetus fOr the development of recombinant DNA and synthetic peptide vaccines for foot and mouth disease. The most important difference between the physiochemical properties of the virions of 4 major genera are the their pH stability. The apthovirus are unstable below pH 7 the rhinoviruses lose activity below pH 5 and entero and cardioviruses are stable at pH 4. The cardioviruses can be distinguished from enteroviruses by their biophasic pH stability in the presence of O.lM halide ions. Another important difference is the presence of polycytidylic acid tract of unknown function in the genome of aptho and cardioviruses but not in entero and rhinoviruses. If protected by mucus and strong sunlight,

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picornaviruses are relatively heat stable. Replication is entirely in the cytoplasm in MORI, T.; MIURA Y.; COTO, Y.; FUJIWARA, Y; HATANO, Y; KODAMA., FUKUYAMA, S.; SASAKI, N. and MATIJMOTO, M., 1976. Epizootic congenital arthrogryposishydranencephaly syndrome in cattle. Insolation of Akabane virus from infected foetuses. Archives of Virology. 51: 57-74. LUPTON, H.W. and PETERS, CJ., 1984. Rift valley fever. Proc. U.S. Animal Health Assoc. 87, 279-290.

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355

MATSUYAMA, T.; OVA, A.; OoATA, T.; KOBAYASHI, I.; NAKAMURA, T.;TAKAHASHI, M. and Kitaoka., M., 1960. Isolation of arboviruses from mosquitoes collected at livestock pens in Gumma Prefecture in 1959. Japn J. Med. Sci. Bio1.l3, 191-198. MATIJMOTO, M. and INABA, Y., 1980. Akabane disease and Akabane virus. Kitasato Arch. Exp. Med. 53, 1-21. MATIJMOTO, M. and INABA, Y., 1980. Akabane disease and Akabane virus. Kitasato Arch. Exp. Med. 53, 1-21. MOHANlY, S.B. and DUITA, S.K., 1981. Veterinary virology, Lea and Febiger, Philadelphia. OVA, A., OKuBO,T., OaATA, T., KOBAYASHI, 1. and MATSuyAMA, T., 1960. Akabane, a new arbovirus isolated in Japan. Jpn. J. Med. Sci. Bio1.14, 101-108. POR1ERFIELD, J.S. and DELLA-PORTA, A.I., 1981. Bunyaviridae: Infections and diagnosis. In E.Kurstak and C.Kurstak (Editors) comparative diagnosis of viral disease. Academic Press, New York, Vol. 4 pp. 479-504. RUSSELL, P.H. and EDINGTON, N., 1985. The Burlington Press (Cambridge) Ltd. Foxton, Cambirdge. The Rift Valley fever, Office International Epizootics Technical Series No.l, 1981.

Chapter 31

Toroviridae

Toroviridae is a newly created family for a group of antigenically related viruses demonstrated in horses, cattle and men. Two new viruses detected in fecal material from horse and cattle in 1982 and 1983 with unique morphological (Latin torus-a doughnut shaped ring), biochemical and serological characters. Toroviruses are enteric viruses recognised in three different species, namely horse, cattle and human beings. Evidence of infection has been obtained in pig, sheep, goat, in lagomorphs and rodents. Toroviruses are enveloped RNA viruses with peplomer bearing envelope and an elongated tubular nucleocapsid of helical symmetry. The nucleocapsid may be bent giving kidney or disk shaped morphology to the virus particle or the neuclocapsid may be straight resulting in rod shaped virion. The genome is single stranded RNA with positive polarity. The moleular weight is about 8 x 106 There are two major proteins in the virus particle, a phosphorylated nucleocapsid polypeptide of 20K and a 22K protein the main constituent of envelope. Additional proteins of 37K and 75-100K range are also present in the virus particle. Toroviruses replicate in the cytoplasm where four subgenomic mRNAs are formed. The replication is dependent on some nuclear function of the host cell. Breda Virus In 1972 a virus was isolated from a rectal swab of horse with diarrhoea in Berne (Switerland). In 1982 Woode et al. described the isolation of virus from epizootic of neonatal calf diarrhoea in Breda,

Toroviridae

357

Iowa. The resemblence of 'Berne virus' and 'Breda virus' particles was described some 10 years later. In 1984 particles resembling Berne virus (BEY) and Breda virus (BRV) in stoqls of adults and children with diarrhoea, which reacted with antibodies against BEV and BRV were described. Properties of the virus: In negatively stained preparations of intestinal contents, faeces or tissue fluids, the virus particles are either elongated or kidney shaped with a diameter of 105-140 x 12-40nm or spherical forms measures 82 nm in diameter; with a pcplomer bearing envelope. The peplomers may be short (7-9 nm) or long (20 nm). Many particles have short stubby peplomers which make the virus easily distinguishable form coronavirus. The jejunal epithelial cells infected with BRV show brick shaped or elongated particles with dimensions 80-100 x 35-42 nm. The BRV has two serotypes BRVl and BRV2. This virus is anligenically related to BEV. BRVl and BRV2 carry common antigens measurable by IF and ELISA. HI has shown clear differences between BRVl and BRV2. BRV possess the haemagglutinating activity. Mouse and rat cells are the only cells agglutinated. The serotype 1 does not elute from erythrocytes while serotypes 2 does. The BRV looses infectivity if faeces are stored at 4C for 2-3 weeks. It is probable that the virus is readily destroyed by disinfectants and heat. The virus does not grow in cell culture. Epidemiology: Breda was isolated from acute enteritis of calf aged 5 days. About 56% of calves in the herd developed diarrhoea in ftrst 20 days -of life. Fifteen percent of calves died. The natural spread of virus takes place by fecal/oral route. The subclinical excretion of rotavirus by sows at parturition has been conftrmed. The bovine dams are considered to be source of neonatal virus infections. There are no reservoir hosts or vectors involved in the spread of virus. The incubation period is as short as 24 hours, experimentally. The serological survey carried out in parts of USA, the Netherlands and Germany by ELISA have shown antibodies against BRV in calf and cow sera to the extent of 85 to 94%. Pathogenesis: The virus fed to colostrum deprived calves or gonotobiotic calves aged 1 hour to 24 days infects the intestine and reaches faeces within 24-72 hours. Diarrhoea or change in appearance of faeces conicides with the virus or change in appeearance of faeces

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conicides with the virus excretion. After recovery the virus can be excreted for atleast 4 months. In colostrum fed calves from immune dams the infection cannot be prevented but symptoms are mild. Viraemia has not been reported. The calves develop anorexia and depression followed within few hours by greenish yellow or yellow diarrhoea. Some calves may show shivering. The signs of dehydration reddening and loss of tone of intestine are noticed. Villus atrophy takes place due to infection of crypt and villus epithelial cells. There is focal necoris and moderate inflammation of the small intestine. Immune reaction: Following primary infection with BRV, the animals develop specific IgM and IgG antibodies. The peak titre is attained 1-2 and 3-4 weeks. The IgA antibodies can also be detected within 2 weeks. The passively derived antibodies do not protect calves from infection. Diagnosis: BRV does not grow in vitro. The EM detection of virus using 3-4% potassium phosphotungstate, pH 7.0, is used to identify ~ virus. The BRV can be distinguished from coronavirus by !EM. Viral haemagglutinin titres of infected calves fecal samples vary from 20,000 to 50,000 while the titre in normal calves is 16-32. ELISA test is used to survey serum antibodies in the herds. Control: There is no specific control measure available as no vaccine has been developed so far. Berne Virus In 1972 a virus was isolated from rectal swab of horse with diarrhoea in Berne (Switzerland). Berne virus (BEV) has been cultured in vitro, in horse kidney cultures. It can also be cultured in other cells of equine origin. In the presence .of actinomycin D and aminitin the BEV replication is drastically reduced when drugs are added during the first 8 hours of infection, indicating that BEV replication depends upon some nuclear funclion of the host cell. The BEV agglutinates the erythrocytes of human '0' group, rabbit and guinea pig but not fJf rat and mouse. The virus shows cross neutralization with Breda virus. There is wide distribution of Berne virus in Swiss horse population and antibodies also occur in sera of cattle, sheep, goats, pigs. laboratory rabbits and two species of wild mice.

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The pathogenic role of BEY has not been proved. It cannot be saidthat BEY was responsible for diarrhoea from the horse it was isolated.

ReferencesHOR2JNBX, M.C.; FLEWETI', T.H.; SAIF, L.I.; SPAAN. I.M.; WEISS, M. and WOOD,O.N., 1987. A new family of vertebrate viruses. Toroviridae Intervirology.27, 17-24.

Wmss, M.; and HORZINEK, M.C., 1987. Theproposedfamily Toroviridae Agents of enteric infections. Arch. Virol. 92, 1-15.Woode. O.N.; Reed, D.E.; RUJUlels, P.L.; Herrig, M.A and Hill, IT., 1982. Studies with an unclassified virus isolated from dimrhoeic calves. Veteminary Microbiology 7: 221-224.WOOD. O.N.; MOHAMMED, K.A.; SAIF, L.J.; WINAND, N.I; QUESADA, M. Kaso, N.E. and POIll.ENZ, IF., 1983. Diagnostic methods for the newly

discovered 'Breda' group of calf enteritis inducing viruses. In: Proceedings of the third sympsosium. World Association of Veterinary Laboratory Diagnosticians pp.533-538.

Chapter 32

Unclassified RNA Virus

Borna Disease VirusBoma discancogenes, 96-98 C>ncoviruses, 323-33 Organ cultures, 51 Orthomyxoviridae virus, 18,30, 278-82 Ovine adenoviruses (OAV). 167-69 Oya, A_,351 Pande, P.G., 238 Papillomaviruses, 94-96 Papovaviridae viruses, 15, 22-23, 159-62 Parainfluenza-l virus, 289

IndexParainfluenza-3 virus. 289-93 Parainfluenza-5 virus. 293 Paramyxovirus. 284-93 Parihar. N.S . 183 Paramyxoviridae viruses. 18,31, 284-306 control, 288-89, 292, 296, 302-03, 306 cultivation, 286, 298 diagnosis, 292, 295-96, 301-02, 306 epidemiology, 286, 290-91, 295, 298-99,305-06 Unrnunereaction,292,301 morbilivirus, 285, 293-305 paramyxovirus, 284-93 pathogenesis, 286-88, 291, 295, 299-301,306pn~ovirus,285,305-06

369Peste-des-petits-ruminants virus, 303-05 Pestivirus, 23845 Picomaviridae virus, 26-27, 213-29 apthovirus, 212-23 control. 222-25, 228-29 cultivation, 214. 224-,28 diagnosis, 218-22, 224-29 enterovirus. 223-28 epidemiology, 215-17, 224-28 irnmunereaction.218 pathogenesis, 217, 224-28 properties of, 212-14,223-24, 226-28 rhinovirus, 228-29 Pigeon herpesvirus, 198 Plaque assay, 52-53 Pneurnovirus,305-06 Pock assay, 53 Polio encephalomyelitis virus, 223-24 Polymerase chain reaction (PCR), 124 Polyomaviruscs, 94-95 Porcine adenoviruscs, 171 Porcine enterovirus-l , 223-24 Porcine enterovirus-9 (PEY -9). 224-25 Porcine herpes virus-I, 191-93 Porcine parvovirus (PPY), 153-54 Pox viruses, see, Poxviridae viruses Poxviridae viruses, 14-15,20-21, 12948 avipox virus, 130, 14648 capripox virus, 129,13841 control, 135-37, 13941, 14345. 14748 cultivation, 131-33, 136-40. 142, 144, 146 diagnosis, 132-33, 135-37. 13940, 142, 144-47 epidemiology, 132, 134, 136-37, 13940, 142, 144-47

properties, 285, 290, 294-95, 292-98,305 Parvoviridae virus, 15,21-22, 150-57 bovine parvoviruses, 151-53 canine parvoviruscs, 156-57 control, 153-54, 156 cultivation, 151, 153, 155 diagnosis, 152-54, 156 epidemiology, 151-52, 154-55 feline panleucopenia virus, 154-56 pathogenesis, 152-54, 156 porcrine parvovirus, 153-54 properties of. 151, 153, 155 Pasteur, Louis, 46,102,313 Pathogenesis of viral infections, 65-75 cytocidal infection, 65-67 non cytocidal infection, 65, 67-68 non cytocidal non productive infection, 65, 67-68 transformation, 66. 68 Persis.tent infections, 67, 76-80

370family, 129-30 immune reaction, 132, 134, 136-37 1eporipox virus, 129, 144-45 orthopoxvirus, 129-38 parapox virus, 129, 144-43 pathogenesis, 132, 134, 136-37, 139-40,143-45,147 properties, 131, 133, 135-36, 138, 140-42, 144-46 suipox virus, 129, 143-44 Proteins, 10-11 Pseudorabies virus, 191-93 Purines antagonists, 108 Pyrarnirdine antagonists, 108 Quantal assay, 53 RNA viruses, bimaviridae. 17, 29,264-66 bunyaviridae, 19.33,347-54 calciviridae. 16-17,27.231-33 coronaviridae, 17,30,267-76 flaviviridae. 17.28,234.247-50 orthomyxoviridae, 18,30.278-82 pararnyxoviridae. 18.31,284-306 picomaviridae, 26-27,211-29 reoviridae. 17,28-29.251-62 retroviridae, 19,32-33.322-45 rhabdoviridae, 18,32.309-20 togaviridae, 17,27-28,234-46 toroviridae, 19.33,356-59 unclassified. 360-61 RNaseL,113 Rabbit papillomaviruses. 162 Rabies virus, 313-18 Radio immunoassay (RIA), 118. 120 Reassortment, 60-61 Remlinger, 313 Reoviridae viruses, 17, 28-29. 251-62

Textbook ofVelerinary Virologycontrol, 253, 256, 262 cultivation, 258-59, 261 diagnosis,253,256, 260 epidemiology, 253, 255-56, 261 Fiji virus, 251 immune reaction, 260 orbiviruses, 251. 257-62 pathogensis,253,256, 259-61 phytoreovirus, 251~perties,252-55,257-58,261

rovirus, 251-54 rotavirus, 251. 254-57 Reovirus, 252-54 Replication groups, 43-44 Replication of viruses, 34-44 Respi!atory viruses 13 Restriction endonuclease digestion of DNA, 122 Retroviridae viruses, 18, 32, 322-45 control, 326, 328-29, 331, 334, 336, 340. 342, 345 diagnosis. 326-29, 331-33, 334, 336, 339, 342, 344 epidemiology, 324-25, 327, 330, 335,337,340-41,343 immune reaction. 326,339,342, 344 lentiviruses, 334-45 oncoviruses,323-33 pathogenesis, 325-32, 334-36. 338-39,341-44 properties, 323-24. 326-30, 332,334-35,337,340,343 spumaviruses, 333-34 Retroviruses, 96-98 Rhabdoviridae virus, 18,31,309-21 bovine ephemeral fever virus, 319-20 control, 312-13, 318, 320 diagnosis,312,317-18,320 epidemiology, 311,315-16,319 immunereaction,312

Indexmarburg virus. 320 pathogenesis. 311-12. 316-17. 319 properties, 310-11. 313-15. 319 rabies virus. 313-18 vesicular stomatis virus, 310-13 Rhinovirus. 228-29 Rickettsia, properties of. 4-5 Rift valley fever virus (RVFV), 348-,51 Rinderpest virus, 296-303 Robbins,49 Rotaviruses. 254-57 Rowe, 164 Rubarth, 169 Sapre, SN., 257 Sarcoma viruses, 326-31 Sorapie, 362-63 Seet.haraman, C.. 217 Sendaivirus,289 Shaila, M.S., 305 Shedding ofvirus, 73-74 Sheep pox virus, 13840 Simian herpes virus-I, 193-94 Singh, 95, 183 Skinner, 215 Slow infection, 78-79 Spwnavirus, 333-34 Stanley, 3 Stoke's law,S Subacute spongiformviral encephalopathies, 78-79 Suspension cultures, 50-51 Swine enteroviruses, 223-25 Swine fever, 24245 Swine influenza virus, 280-81 Swine pox virus, 143-44 Swine vesicular disease virus, 224-25 Talf" dis~e, 223-24 Teschan virus 223-24 Thiosemicarbazones, 108 Togaviridae viruses, 17,27-28,

371

234-46alphaviruses, 235-38 arterivirus, 245-46 control, 23~, 240-42, 244-46 diagnosis, 237, 240, 242. 24446 epidemiology, 237, 239, 241, 243,245 family of, 236 flaviviridae and, 234 bmununereaction,240 pathogenesis, 237, 23940 pestivirus,23845 properties of, 236-38, 241, 243. 245 Toroviruses,19 Toumier,4 Transformation assay, 53 Transmissble gastroenteritis virus (l'GEV), 272-73 Trautwein, K., 214 Tubular symmetry, 7-8 Tumor viruses, effect of interferon on transformation by, 113-14 families, 94-96 oncogenes, 96-98 retroviruses, 96-101 transformation of genes, 96-98 Twort, 3 Unicellular organism, properties of, 4-5 Vaccinia virus, 131-33 Varet monkey disease, 320 Vasudeven, D.W., 257 Vesicular disease diagnosis, 219 Vesicular exanthema virus (VEV),231-32 Vesicular stomatis virus (VS V), 310-13

372Viral disease, diagnosis of, 115-25 material for, 115-16 molecular biological techniques, 122-25 serological methods, 118-22 viral nucleic acid detection, 122 virus isolation 117-18 visualisation by election microscope, 116-17 epidemiology of, 87-92, 124 dissemination of virus, 91-92 environmental factors, 89 host agent, 89 incubation period of vi~s, 91-92 perpetuation of viruses, 89-90 tools, 87-88 transmission of viruses, 90-92 viral agent 88 Viral envelope, 8 Viral genetics, 55-63 genes in viruses, 58 genome, 57-59 marker rescue, 60, 62 mutation, 56-57 reactivation, 60 restricted endonuclease cleavage maps, 60, 62-63 viruses recombination, 59-60, 63 Viral genome replication, 40-43 Viral immunity, 81-85 antibody effect, 82-83 cell mediated immunity, 83 cytotoxic T cells 83-85 humoral response, 82 infection, 81-82 Viral infectivity assay, 52-53 Viral protein, cytopathic effect of, 66 Viral replication, 34-44 Viral synthesis, 37-38 Viral vaccines, antiviral drugs, 107-08

TexJbook o/Veterinary Virologyattenuated, 102-05 categories, 102-06 inactivated, 102, 104-06 inhibitors, 108-09 interferences, 109-14 biological effects,1l1-13' clinical use, 114 prod~tion of, 111 tumor virus and,113-14 types of, 110 isolated irnmunogenes, 106-07 Virion assembly, 43 Viroiogy, divisions of, 3 see Viruses Virus neutralization test (VN), 118-19 Virus protein synthesis, 40 Viruses, chemical structure, 8-12 classification, 13-33 cultivation, 44-54 DNA viruses, 14-16,20-26, 129-208 detection and identification, 124-25 diseases, 82-92, 115-25 dissemination, 91-92 entry to animal body, 88-72 genes, 58 genetics, 11-12,55-63 immunity,81.85 incubation period, 91-92 morphology, 5-8 pathogenesis, 65-75 perpetuation of, 89-90 physical structure, 5-8 properties, 4-5 RNA viruses, 16-19,26-33, 211-361 replication, 34-44 see also specific vi.,.ses

Indexshedding, 73-74 sized,4-5 sprelld of, 68-72 transmission of, 90-92 tumorogenesis !Lid, 94-101 vaccines, 102-14 Visna virus, 78, 337-40 Waldman, D., 214 Warfield, 151 WeBer, 49 Wesselsbom virus, 249 Woodruff,47 Zinke, 313

373