* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download What are Viruses?
Foot-and-mouth disease wikipedia , lookup
Avian influenza wikipedia , lookup
Hepatitis C wikipedia , lookup
Elsayed Elsayed Wagih wikipedia , lookup
Human cytomegalovirus wikipedia , lookup
Taura syndrome wikipedia , lookup
Canine distemper wikipedia , lookup
Orthohantavirus wikipedia , lookup
Marburg virus disease wikipedia , lookup
Influenza A virus wikipedia , lookup
Canine parvovirus wikipedia , lookup
Hepatitis B wikipedia , lookup
Aquaculture Viruses What a Virus Isn’t • Not a bacterium • not an independently-living organism • cannot survive in absence of a living cell within which to replicate • antibiotics do no harm to a virus, unless indirectly • treatment of a flu virus with antibiotics is only the treatment of its symptoms • you don’t kill the organism that causes the flu What are Viruses?: an Introduction • Infectious agents composed mainly of nucleic acid with a protein coat (capsid) • can only be seen with an electron microscope • range in size from 10 to 200 nanometers (nM) • carry on normal cell-like function unless free, then infectious • in infectious form, they neither grow nor respire • can enter living plant, animal or bacterial cell What do Viruses Look Like? • Most viruses have a capsid, core and genetic material (DNA/RNA) • capsid: outer shell of the virus which encloses genetic material (link: chemical structure of capsid helps determine immune response to virus) • capsid is made of many identical individual proteins, precisely assembled • protein core under capsid protecting genetic material • sometimes an additional covering (lipid bilayer w/embedded proteins) on outside known as an envelope • resembles a baseball • various forms: rods, filaments, spheres, cubes, crystals Virus Appearance: capsid capsomere: unit/molecule associated with capsid structure Typical Virus Shapes SPHERES RODS CUBES More Virus Shapes Composition of T-Even Bacteriophage • Capsid: brains of virus, tightly-wound protein protecting nucleic acids • Body: attached to capsid head, rod-like structure w/retractible sheath, hollow core • Tail: at end of core is a spiked plate carrying 6 slender tail fibers, anchor virus to its host What are Viruses?: an Introduction • Viruses make use of the host cell’s chemical energy, protein and nucleic acid synthesizing ability to replicate themselves • bacteriophage: infect the host through a tail-like adaptation • each virus attacks a specific type of cell • cold viruses attack cells of the lung • the AIDS virus attacks T4 cells of the immune system Bacteriophage Attack What are Viruses?: an Introduction • Viral nucleic acids are single- or double- stranded and may be DNA and RNA • after viral components are made by the infected host cell, viral particles are released • often, the virus alters the intracellular environment enough to damage or kill the cell • if enough cells are destroyed, disease results • some viruses do not kill cells, but transform them into a cancerous state, remaining latent for a long time Role of RNA/DNA • Supplies the codes for building the protein coat (capsid) and for producing enzymes needed to replicate more viruses • codes also provide enzymes that allow the newly-built viruses to lyse cells (e.g., bacteriophage) • cell is ruptured and destroyed What do Viruses Actually Do? • All viruses only exist to make more viruses • all, with the exception of some bacterial viruses, appear to be harmful • their replication leads to the death of the cell which the virus has entered • virus enters the cell by first attaching a specific structure on the cell’s surface • depending on the virus, either the entire virus enters the cell or only the genetic material is injected The Virus Invasion • Phase 1: spike and fibers attach themselves to the walls of the cell or bacteria • Phase 2: the sheath contracts and drives the core through the cell wall (injection) • Phase 3: the nucleic acid passes through the core, from the capsid head, into the host cell • Phase 4: nucleic acid disappears, afterwards (10m) hundreds of virions appear causing the cell to rupture, releasing hundreds of small viral replicates • this is how it can replicate so quickly The Virus Invasion What Things Can Become Infected by a Virus? • All living things have some susceptibility to a particular virus • virus is specific for the organism • within a species, there may be a 100 or more different viruses which can affect that species alone • specific: for example, a virus that only affects one organism (humans and smallpox) • influenza can infect humans and two animals Different Types of Viruses • Major classification: animal, plant, bacterial • Sub-classified by arrangement and type of nucleic acid • animal virus group: double-stranded DNA, singlestranded DNA, double-stranded RNA, singlestranded RNA, retrovirus • influenza: SS-RNA • for all viruses, regardless of the kind of arrangement of genetic material, the virus is capable of replicating within a living cell and can produce progeny Do Viruses ever Change? • Sometimes during viral replication, mutations occur • if the mutation is harmful, the new virus particle might no longer be functional (infectious) • however, because a given virus can generate many, many copies, a small number of non-functional viruses is not important • mutation is not necessarily damaging to the virus -it can lead to a functional but new strain of virus Defense Against Viruses • First Line: skin and mucous membrane, which also lines the gastrointestinal and respiratory passageways • skin is tough and stomach acidity acts as a disinfectant • Second Line: after the virus enters the blood and other tissues, white blood cells and related cells (phagocytes) consume them • accumulation of phagocytes in area of infection is known as “puss” Defense Against Viruses Antibodies attacking chickenpox virus Defense Against Viruses • Antibodies are the best defense against viruses • unfortunately, they are specific in their action • chickenpox antibody will only attack a chickenpox virus • a particular virus stimulates the production of a particular antibody Defense Against Viral Infection • Humans are protected in a couple of ways: • 1) intracellular: if a particular virus attacks cells, our bodies produce interferons • interferons (alpha, beta or gamma) are proteins which interact with adjacent cells and cause them to become more resistant to infection by the virus • if the resistance is not quite good enough, we become sick Defense Against Viral Infection • 2) immune system (extracellular): kills the virus outside the cell • also kills the infected cells • virus cannot spread • eventually the virus is completely removed and we get better • exception: HIV because it infects cells of the immune system, itself • chemicals/drugs: acyclovir, AZT, HIV protease inhibitor Major Viral Infections in Fish • • • • Infectious pancreatic necrosis (IPN) Viral hemorrhagic septicemia (VHS) Infectious hematopoetic necrosis (IHN) Channel catfish virus disease (CCVD) (1) Infectious Pancreatic Necrosis (IPN) • Acute, viral infection of salmonids, especially trout and char • causes high mortality in fry, sometimes fingerlings, rare in larger fish • isolated in Pacific NW in 1960’s, wiped out brook trout in Oregon in 1971-73 • classified as a reo-like virus • only 65 nM in diam, smallest of fish viruses IPN: general notes • Single capsid shell, icosohedral symmetry, no envelope • contains two segments of DS-RNA • fairly stable and resistant to chemicals (acid, ether, etc.), variable resistance to freezing • remains infectious for 3 months in water • causes general viremia, but targets pancreas and hematopoietic tissues of kidney/spleen IPN: epizootiology • Host/geographic range: all salmonids, brook trout most susceptible, report from various marine fish (flounder) and some inverts • Reservoirs: carriers, once a carrier always a carrier, virus particles shed in feces/urine • Transmission: horizontal, by waters via carriers or infected fry; vertical from adults to progeny; experimentally by feeding infected material, IP injection • Pathogenesis: entry via gills, digestive tract • Environmental factors: mortality reduced at lower temps (carrier not reduced) IPN: pathology • Gross external: sudden mortality in fry, largest affected first, whirling, rotating, lethargy, exophthalmia, hemorhrhages at base of fins • Gross internal: petechae of pyloric cecae (small spot on surface of membrane, caused by localized hemorraging), muscle, viscera; pale liver, spleen, no food in digestive tract • Histopathology: necrosis of pancreatic cells, mild necrosis of kidney tissue, intestinal lining IPN: detection, diagnosis and control • Isolation: whole fry, kidney, spleen, pyloric cecae, sex fluids are all good sources • Presumptive tests: epizootiological evidence and/or typical PCE in infected cells • Definitive tests: serology (FAT, serum neutralization) • Control: avoid virus in water, virus-free stock, destruction of infected stock, some vaccination possible in future (2) Viral Hemorrhagic Septicemia (VHS) • • • • Viral disease of European salmonids recognized in Denmark in 1949 isolated from Pacific Coast in 1989 rhabdovirus, bullet-shaped (one rounded end), 185 x 65 nM, lipoprotein envelope • non-segments SS-RNA • sensitive to ether and chloroform, heat, acid • resistant to freeze-drying Viral Hemorrhagic Septicemia • Produces a general viremia, tissue and organ damage, liver necrosis, spleen, kidney • epizootiology: cultured rainbow trout, also brown trout, steelhead, chinook, coho • mainly found in Washington state • reservoirs: survivors are life-long carriers, usually rainbow trout, brown in Europe • transmission: horizontal through water, virus can occur on eggs spawned by carriers, IP injection, birds, hatchery equip Viral Hemorrhagic Septicemia (VHS) • Pathogenesis: infection results in viremia, disrupts many organ systems, 200-300g fish most affected • Environmental factors: low temp (< 8oC) • External pathology: lethargis, hanging downward in water, swimming in circles, exopthalmia, dark discoloration, hemorrhages in roof of mouth, pale gills w/focal hemorrhages Viral Hemorrhagic Septicemia (VHS) • Internal pathology: gut devoid of food, liver pale, hemorrhages in connective tissue, kidney gray and swollen (chronic), red and thin (acute) • Histopathology: necrosis of liver, kidney nephrons, spleen, pancreas, melanin in kidneys and spleen • Isolation/tests: isolated from kidney/spleen, epizootiological evidence, CPE isolation, definitive test is serum neutralization or fluorescent antibody Viral Hemorrhagic Septicemia (VHS) External hemorrhages Internal hemorrhages Liver red in acute stage Viral Hemorrhagic Septicemia • Prevention: clean broodstock, water = fish, avoid infected broodstock, test and slaughter • can spread very quickly from farm to farm: avoid close proximity to other farms • vaccines are under development Infectious Hematopoetic Necrosis (IHN) • Salmon and trout, 100 million mortalities between 1970-1980, 70% mortality • agent: bullet shaped rhabdovirus, non- segmented SS-RNA, sensitive to heat and pH, glycoprotein is spiked on surface of virus • host/range: sockeye, chinook, rainbows; cohos resistant; mortality in young fish; spread by shipment Infectious Hematopoetic Necrosis (IHN) • Reservoirs: survivors become life-long carriers, adults shed virus at spawning • transmission: horizontal, primary mode is vertical via ovarian fluid (virus hitches ride on sperm into egg); feeding and inoculation have worked experimentally • pathogenesis: gills suspected; incubation period depends on temp, route, dose, age; fry most susceptible; extensive hemorrhaging, necrosis of many tissues; death usually due to kidney failure Infectious Hematopoetic Necrosis (IHN) • Environmental factors: temp very important, slows below 10 C, holding in tanks/handling increase severity • External pathology: lethargy, whirling, dropsy, exopthalmia, anemia, hemorrhaging of musculature/fins, scoliosis • Internal pathology: liver, kidney, spleen pale; stomach/intestines filled with milky fluid; petechial hemorrhaging • Histopathology: extensive necrosis of hematopoetic tissue of kidney/spleen Infectious Hematopoetic Necrosis (IHN) • Definitive diagnosis: serum neutralization, FAT, ELISA • Prevention: avoidance, quarantine, clean water with UV, ozone, virus-free stock; test, slaughter, disinfect; disinfect eggs; vaccines under development; elevated water temp Channel Catfish Virus Disease (CCVD) • Contagious herpes virus affecting only channel catfish less than four months old • occurs in SE United States, California, Honduras • acute hemorrhagia, high mortality, first discovered in 1968 • agent: enveloped capsid, icosohedral nucleocapsid with 162 capsomeres • physio/chemical properties: easy to kill, sensitive to freeze-thaw, acid, ether, etc. Channel Catfish Virus Disease (CCVD) • Environmental factors: optimal temperature 28-30 C, common during warmer months, cooler water = big difference • epizootiology: horizontal, vertical suspected • external pathology: spiral swimming; float with head at surface; hemorrhagic fins, abdomen; ascites; pale or hemorrhagic gills; exophthalmia Channel Catfish Virus Disease (CCVD) • Internal pathology: hemorrhages of liver, kidney, spleen, gut, musculature; congestion of mesenteries and adipose • Histopathology: necrosis of kidney, other organs; macrophages in sinusoids of liver, etc.; degeneration of brain • Presumptive diagnosis: clinical signs, epizootiological evidence, CPE • Definitive diagnosis: serum neutralization, fluorescent antibody Channel Catfish Virus Disease (CCVD) • Prevention: avoid potential carriers (survivors) or infected fry, keep temperature below 27oC (will still produce carriers), attenuated vaccine shows some promise • Therapy: none available Channel Catfish Virus Disease Channel Catfish Virus Disease