MEDICALLY IMPORTANT VIRUSES - Dspace.zsmu.edu.ua
MINISTRY OF HEALTH SERVISE OF UKRAINEZAPORIZHZHYA STATE MEDICAL UNIVERSITYTHE CHAIR OF MICROBIOLOGY, VIROLOGY, IMMUNOLOGYMEDICALLY IMPORTANT VIRUSESThe methodical manual for medical studentsZaporizhzhya20151
УДК 578(075. 8) 111ББК 52.64Я73E70Guidelines ratified on meeting of the Central methodical committee ofZaporizhzhya state medical university (protocol numbers 2 (26.09.2015) and it isrecommended for the use in educational process for foreign students.REVIEWER: Popovich A.P., docent of the Chair of Medical BiologyAUTHORS:Yeryomina A.K., senior lecturer of the chair of microbiology, virology andimmunology, candidate of Biological Sciences.Kamyshny A.M., the heat of the chairof microbiology, virology, and immunology,doctor of medicine.Kirsanova E.V., assistant professor of the chair gygien and ecology, candidate ofMedicine.Sukhomlinova I. E., senior lecturer of the chair of normal physiology, candidate ofMedicine.Medically important viruses : the methodical manual for medical students /A. K. Yeryomina [et al.]. – Zaporizhzhya: [ZSMU], 2015. – 75 p.The independent practical work of students is an important part of the syllabus in thecourse of microbiology, immunology. It helps students to study this fundamental subject.The systematic independent work enables to reach the final goal in the students’education. It is also important while preparing the students for their future clinic workwith patients. These theoretical material, questions and tests help students to get ready forexamination.The methodical manual for practical lessons on microbiology, virology,immunology for the medical students of ІІ -ІІІ year of the study are approved by theCentral Methods Board of ZSMU as a methodical manual on practical lessons for studentsof the medical faculty.2
CONTENSDNA ENVELOPED VIRUSES 4DNA NONENVELOPED VIRUSES .10RNA ENVELOPED VIRUSES.11RNA NONENVELOPED VIRUSES 20SLOW DISEASES CAUSED BY PRIONS .24Practical class # 1 29Practical class # 2 32Practical class # 3 34Practical class # 4 36Practical class # 5 40Practical class # 6 42Practical class # 7 45Practical class # 8 49Quizzes .53Correct answers .763
DNA ENVELOPED VIRUSESHerpes Simplex Virus Type 1Diseases: Herpes labialis (fever blisters or cold sores), keratitis, encephalitis.Characteristics: Enveloped virus with icosahedral nucleocapsid and lineardouble-stranded DNA. (Fig. 1.). No virion polymerase. One serotype; crossreaction with HSV-2 occurs. No herpes group-specific antigen.CapsomerDNRTegumentCapsidEnvelopFig. 1. Structure of Herpes Simplex VirusTransmission: By saliva or direct contact with virus from the vesicle.Pathogenesis: Initial vesicular lesions occur in the mouth or on the face.The virus then travels up the axon and becomes latent in sensory (trigeminal)ganglia. Recurrences occur in skin innervated by affected sensory nerve and areinduced by fever, sunlight, stress, etc.Dissemination occurs in patients with depressed cell-mediated immunity.Laboratory Diagnosis: Virus causes cytopathic effect (CPE) in cell culture.4
It is identified by antibody neutralization or fluorescent-antibody test.Tzanck smear of cells from the base of the vesicle reveals multinucleated giantcells with intranuclear inclusions.These giant cells are not specific for HSV-1; they are seen in the vesicularlesions caused by HSV-2 and varicella-zoster virus as well.A rise in antibody titer can be used to diagnose a primary infection but notrecurrences. Intranuclear inclusions seen in infected cells. HSV encephalitis can bediagnosed using a PCR assay to detect HSV-1 DNA in spinal fluid.Treatment: Acyclovir for encephalitis and disseminated disease. Acyclovirhas no etiect on the latent state of the virus.Trifluorothymidine for keratitis. Primary infections and localized recurrencesare self-limited. A variety of over-the-counter drying agents can be used to promotehealing.Prevention: Recurrences can be prevented by avoiding the specific incitingagent such as intense sunlight. Acyclovir can reduce recurrences. No vaccine isavailable.Herpes Simplex Virus Type 2Diseases: Herpes genitalis, aseptic meningitis, and neonatal infection.Characteristics: Enveloped virus with icosahedral nucleocapsid and lineardouble-stranded DNA. No virion polymerase. One serotype; cross-reaction withHSV-1 occurs. No herpes group-specific antigen.Transmission: Sexual contact in adults and during passage through the birthcanal in neonates.Pathogenesis: Initial vesicular lesions occur on genitals. The virus then travelsup the axon and becomes latent in sensory (lumbar or sacral) ganglion cells.Recurrences may be induced by stress.Laboratory Diagnosis: Virus causes CPE in cell culture. Identify by antibodyneutralization or fluorescent-antibody test. Tzanck smear reveals multinucleatedgiant cells but is not specific for HSV-2. A rise in antibody titer can be used todiagnose a primary infection but not recurrences.5
Treatment: Acyclovir is useful in the treatment of both primary and recurrentdisease. It has no effect on the latent state.Prevention: Primary disease can be prevented by protection from exposure tovesicular lesions. Recurrences can be reduced by the long-term use of oral acyclovir.There is no vaccine.Varicella-Zoster VirusDiseases: Varicella (chickenpox) in children and zoster (shingles) in adults.Characteristics: Enveloped virus with icosahedral nucleocapsid and lineardouble-stranded DNA. No virion polymerase. One serotype.Transmission: Varicella is transmitted primarily by respiratory droplets.Zoster is not transmitted; it is caused by a reactivation of latent virus.Pathogenesis: Initial infection is in the respiratory tract. It spreads via theblood to the internal organs such as the liver and then to the skin.After the acute epispde of varicella, the virus remains latent in the sensoryganglia and can reactivate to cause zoster years later, especially in older and immunocompromised individuals.Laboratory Diagnosis: Virus causes CPE in cell culture and can be identifiedby fluorescent-antibody test. Multinucleated giant cells seen in smears from the baseof the vesicle. Intranuclear inclusions seen in infected cells. A 4-fold rise in antibodytiter in convalescent-phase serum is diagnostic.Treatment: No antiviral therapy is indicated for varicella or zoster in theimmunocompetent patient. In the immunocompromised patient, acyclovir canprevent dissemination.Prevention: Vaccine contains live, attenuated virus. Immunocompromisedpatients exposed to the virus should receive passive immunization with varicellazoster immune globulin (VZIG) and acyclovir to prevent disseminated disease.CytomegalovirusDiseases: Cytomegalic inclusion body disease in infants. Mononucleosis intransfusion recipients. Pneumonia and hepatitis in immunocompromised patients.6
Characteristics: Enveloped virus with icosahedral nucleocapsid and lineardouble-stranded DNA. No virion polymerase. One serotype.Transmission: Virus is found in many human body fluids, including blood,saliva, semen, cervical mucus, breast milk, and urine.It is transmitted via these fluids, across the placenta, or by organ transplantation.Pathogenesis: Initial infection usually in the oropharynx. In fetal infections,the virus spreads to many organs, eg, central nervous system and kidneys. In adults,lymphocytes are frequently edinfectioninimmunocompromised patients can result from either a primary infection orreactivation of a latent infection.Laboratory Diagnosis: The virus causes CPE in cell culture and can beidentified by fluorescent-antibody test. "Owl's eye" nuclear inclusions are seen. A 4fold rise in antibody titer in convalescent-phase serum is diagnostic.Treatment: Ganciclovir is beneficial in treating pneumonia and retinitis.Acyclovir is ineffective.Prevention: No vaccine is ayailable. Ganciclovir suppresses retinitis. Do nottransfuse CMV antibody-positive blood into newborns or antibody-negativeimmunocompromised patients.Epstein-Barr VirusCharacteristics: Enveloped virus with icosahedral nucleocapsid and lineardouble-stranded DNA. No virion polymerase. One serotype.Transmission: Virus found in human oropharynx and В lymphocytes. It istransmitted primarily by saliva.Pathogenesis: Infection begins in the pharyngeal epithelium, spreads to thecervical lymph nodes, then travels via the blood to the liver and spleen.Laboratory Diagnosis: The virus is rarely isolated. Lymphocytosis, includingatypical lymphocytes, occurs. Heterophil antibody is typically positive (Monospottest). A significant rise in EBV-specific antibody to viral capsid antigen isdiagnostic.7
Treatment: No effective drug is available.Prevention: There is no drug or vaccine.Hepatitis В VirusDiseases: Hepatitis B; implicated as a cause of hepatocellular carcinoma.Characteristics: Enveloped virus with incomplete circular double-strandedDNA; ie, one strand has about one-third missing and the other strand is "nicked"(not covalently bonded). DNA polymerase in virion. HBV-encoded polymeraseacts as a reverse transcriptase by using viral mRNA as the template for the synthesisof progeny genome DNA.There are three important antigens: the surface antigen, the core antigen, and thee antigen, which is located in the core. In the patient's serum, long rods andspherical forms composed solely of HBsAg predominate. HBV has one serotypebased on the surface antigen.Transmission: Transmitted by blood, during birth, and by sexual intercourse.Pathogenesis: Hepatocellular injury due to immune attack by cytotoxic (CD8)T cells. Antigen-antibody complexes cause arthritis, rash, and glomerulonephritis.About 5% of HBV infections result in a chronic carrier state.Chronic hepatitis and cirrhosis can occur. Hepatocellular carcinoma may berelated to the integration of part of the viral DNA into hepatocyte DNA.Laboratory Diagnosis: HBV has not been grown in cell culture.Three serologic tests are commonly used: surface antigen (HBsAg), surfaceantibody (HBsAb), and core antibody (HBcAb). Detection of HbsAg for more than6 months indicates a chronic carrier state.The presence of e antigen indicates a chronic carrier who is making infectiousvirus.Treatment: No specific treatment.Prevention: There are three main approaches: (1) vaccine that containsHBsAg as the immuno-gen; (2) hyperimmune serum globulins obtained fromdonors with high titers of HBsAb; and (3) education of chronic carriers regardingprecautions.8
Smallpox VirusDisease: Smallpox (eradicated in 1980).Characteristics: Poxviruses are the largest viruses. Enveloped virus with lineardouble-stranded DNA. DNA-dependent RNA polymerase m virion. One serologictype. (Fig. 2.).Fig. 2. Pocks on the choriollantoic membraneof the chick embryo, infected by small pox viruses.Transmission: By respiratory droplets or direct contact with the virus fromskin lesions.Pathogenesis: The virus infects the mucosal cells of the upper respiratorytract, then spreads to the local lymph nodes and by viremia to the liver and spleenand later the skin. Skin lesions progress in the following order: macule, papule,vesicle, pustule, crust.Laboratory Diagnosis: Virus identified by CPE in cell culture or "pocks" onchorioallantoic membrane.Electron microscopy reveals typical particles; cytoplasmic inclusions seen inlight microscopy.Viral antigens in the vesicle fluid can be detected by precipitin tests. A 4-fold or9
greater rise in antibody titer in the convalescent-phase serum is diagnostic.Treatment: None.Prevention: Vaccine contains live attenuated vaccinia virus. Vaccine is nolonger used except by the military, because the disease has been eradicated.DNA NONENVELOPED VIRUSAdenovirusDiseases: Upper and lower tract respiratory disease, especially pharyngitis andpneumonia. Enteric strains cause diarrhea. Some strains cause sarcomas in certainanimals but not humans.Characteristics: Nonenveloped virus with icosahedral nucleocapsid and lineardouble-stranded DNA. No virion polymerase. (Fig. 3.).FibrePeptone baseDNRPeptoneHexonFig. 3. Structure of adenovirusesThere are 34 serotypes, some associated with specific diseases.Transmission: Respiratory droplet primarily; iatrogenic transmission in eyedisease.Pathogenesis: Virus preferentially infects epithelium of respiratory tract andeyes. After acute infection, persistent, low-grade virus production withoutsymptoms can occur in the pharynx.10
Laboratory Diagnosis: Virus causes CPE in cell culture and can be identifiedby fluorescent-antibody or complement fixation test. Antibody titer rise inconvalescent-phase serum is diagnostic.Treatment: None.Prevention: Live vaccine against types 3,4, and 7 is used in the military toprevent pneumonia.RNA ENVELOPED VIRUSESInfluenza VirusDisease: Influenza. Influenza A virus is the main cause of world-wideepidemics (pandemics).Characteristics: Enveloped virus with a helical nucleocapsid and segmented,single-stranded RNA of negative polarity. RNA polymerase in virion.The two major antigens are the hemagglutinin and the neuraminidase onseparate surface spikes. Antigenic shift in these proteins as a result of re-assortmentof RNA segments accounts for the epidemics of influenza caused by influenza Avirus.Influenza A viruses of animals are the source of the new RNA segments.Antigenic drift due to mutations also contributes. The virus has many serotypesbecause of these antigenic shifts and drifts.The antigenicity of the internal capsid protein determines whether the virus isan A, B, or С influenza virus. (Fig. 4).11
HemagglutininNeuromenidaseEnvelopeRNAProteinsFig. 4.Influenza virusTransmission: Respiratory droplets.Pathogenesis: Infection is limited primarily to the epithelium of the respiratorytract.Laboratory Diagnosis: Virus grows in cell culture and embryonated eggs andcan be detected by hemadsorption or hemagglutination. It is identified byhemagglutination inhibition or complement fixation.Antibody titer rise in convalescent-phase serum is diagnostic.Treatment: Amantadine is available but infrequently used.Prevention: Vaccine contains inactivated strains of A and В virus currentlycausing disease.The vaccine is not a good immunogen and must be given annually.Recommended for people older than age 65 years and for those with chronicdiseases, especially of the heart and lungs.Amantadine provides good prophylaxis in unvaccinated people who have beenexposed.Measles Virus12
Disease: Measles. Subacute sclerosing panencephalitis is a rare latecomplication.Characteristics: Enveloped virus with a helical nucleocapsid and one piece ofsingle-stranded, negative-polarity RNA. RNA polymerase in virion. It has a singleserotype.Transmission: Respiratory droplets.Pathogenesis: Initial site of infection is the upper respiratory tract. Virusspreads to local lymph nodes and then via the blood toother organs, including the skin. Giant cell pneumonia and encephalitis canoccur. The maculopapular rash is due to cell-mediated immune attack by cytotoxicT cells on virus-infected vascular endothelial cells in the skin.Laboratory Diagnosis: The virus is rarely isolated. Serologic tests are usedif necessary. Treatment: No antiviral therapy is available.Prevention: Vaccine contains live attenuated virus. Usually given incombination with mumps and rubella vaccines.Mumps VirusDisease: Mumps. Sterility due to bilateral orchitis is a rare complication.Characteristics: Enveloped virus with a helical nucleocapsid and one piece ofsingle-stranded, negative-polarity RNA. RNA polymerase in virion. It has a singleserotype.Transmission: Respiratory droplets.Pathogenesis: The initial site of infection is the upper respiratory tract.The virus spreads to local lymph nodes and then via the bloodstream to otherorgans, especially the parotid glands, testes, ovaries, meninges, and pancreas.Laboratory Diagnosis: The virus can be isolated in cell culture and detectedby hemadsorption. Diagnosis can also be made serologically.Treatment: No antiviral therapy is available.Prevention: Vaccine contains live attenuated virus. Usually given incombination with measles and rubella vaccines.13
Rubella VirusDisease: Rubella. Congenitalrubella syndrome is characterized bydevelopmental malformations, especially cardiovascular and neurologic, and byprolonged virus excretion.Characteristics: Enveloped virus with an icosahedral nucleocapsid and onepiece of single-stranded positive-polarity RNA. No polymerase in virion. It has asingle serotype.Transmission: Respiratory droplets and across the placenta from mother tofetus.Pathogenesis: The initial site of infection is the nasopharynx, from which itspreads to local lymph nodes.It then disseminates to the skin via the bloodstream. The rash is attributed toboth viral replication and immune injury.During maternal infection, the virus replicates in the placenta and then spreadsto fetal tissue. If infection occurs during the first trimester, a high frequency ofcongenital malformations occurs.Laboratory Diagnosis: Virus growth in cell culture is detected byinterference with plaque formation by coxsackievirus; rubella virus does not causeCPE.To determine whether an adult woman is immune, a single serum specimen todetect IgG antibody in the hemagglutination inhibition test is used.To detect whether recent infection has occurred, either a single serum specimenfor IgM antibody or a set of acute- and convalescent-phase sera for IgA antibodycan be used.Treatment: No antiviral therapy is available.Prevention: Vaccine contains live attenuated virus. Usually given incombination with measles and mumps vaccine.Parainfluenza VirusDisease: Bronchiolitis in infants, croup in young children, and the commoncold in adults.14
Characteristics: Enveloped virus with helical nucleocapsid and one piece ofsingle-stranded, negative-polarity RNA. RNA polymerase in virion.Unlike influenza viruses, the antigenicity of its hemagglutinin andneuraminidase is stable. There are four serotypes.Transmission: Respiratory droplets.Pathogenesis: Infection and death of respiratory epithelium without systemicspread of the virus. Multinucleated giant cells caused by the viral fusion protein area hallmark.Laboratory Diagnosis: Isolation of the virus in cell culture is detected byhemadsorption. Im-munofluorescence is used for identification.A 4-fold or greater rise in antibody titer is diagnostic in primary infections, butthe heterotypic response limits its usefulness in repeated infections.Treatment: None.Prevention: No vaccine or drug is available.Respiratory Syncytial VirusDiseases: Bronchiolitis and pneumonia in infants. Otitis media in olderchildren.Characteristics: Enveloped virus with a helical nucleocapsid and one piece ofsingle-stranded, negative-polarity RNA. RNA polymerase in virion.Unlike other paramyxoviruses, it has only a fusion protein in its surface spikes.It has no hemagglutinin.It has a single serotype.Transmission: Respiratory droplets.Pathogenesis: Infection involves primarily the lower respiratory tract ininfants without systemic spread.Immune response probably contributes to pathogenesis.Laboratory Diagnosis: Isolation in cell culture. Multinucleated giant cellsvisible. Immunofluo-rescence is used for identification.Serology is not useful for diagnosis in infants.15
Treatment: Aerosolized ribavirin for sick infants.Prevention: No vaccine or prophylactic drug isavailable.Rabies VirusDisease: Rabies.Characteristics: Bullet-shaped enveloped virus with a helical nucleocapsidand one piece of single-stranded, negative-polarity RNA.RNA polymerase in virion. The virus has a single serotype.Transmission: Animal bite, usually by wild animals such as skunks, raccoons,and bats.In the United States, dogs are infrequently involved, but in developingcountries they are often involved.Pathogenesis: Viral receptor is the acetylcholine receptor on the neuron.Replication of virus at the site of the bite, followed by ascension up the nerve to thecentral nervous system.After replicating in the brain, the virus migrates peripherally to the salivaryglands, where it enters the saliva.When the animal is in the agitated state as a result of encephalitis, virus in thesaliva can be transmitted via a bite.Laboratory Diagnosis: Tissue can be stained with fluorescent antibody orwith various dyes to detect inclusions called Negri bodies.The virus can be isolated in newborn mice, but because this procedure takes 1 or2 weeks, it cannot be used to determine whether a person should receive thevaccine.Serologic testing is useful only to make the diagnosis in the clinically ill patient;it does not help the person who has been bitten. It is also used to evaluate theantibody response to the vaccine given before exposure to those in high-riskoccupations.Treatment: No antiviral therapy is available.Prevention: Preexposure prevention of rabies consists of the vaccine only.16
Postexposure prevention consists of (1) washing the wound; (2) giving immuneserum, mostly into the wound; and (3) giving the inactivated vaccine made inhuman cell culture.The decision to give the immune serum and the vaccine depends on thecircumstances.Prevention of rabies in dogs and cats by using a killed vaccine has reducedhuman rabies significantly.Human Immunodeficiency VirusDisease: Acquired immunodeficiency syndrome (AIDS).Characteristics: Enveloped virus with two copies (diploid) of a singlestranded, positive-polarity RNA genome. RNA-dependent DNA polymerase(reverse transcriptase) makes a DNA copy of the genome, which integrates into hostcell DNA.Precursor polypeptides must be cleaved by virus-encoded protease to producefunctional viral proteins.The tat1 gene encodes a protein that activates viral transcription.It is a type D retrovirus (lentivirus). Antigenicity of the gpl20 protein changesrapidly; therefore, there are many serotypes. (Fig. 5).17
Reverse transcriptaseEnvelopCoreFig. 5.RNAStructure of HIVTransmission: Transfer of body fluids, eg, blood and semen. Alsotransplacental and perinatal transmission.Pathogenesis: Two receptors are required for HIV to enter cells.One receptor is CD4 protein found primarily on helper T cells. HIV infects andkills helper T cells, which predisposes to opportunistic infections.Other cells bearing CD4 proteins on the surface, eg, astrocytes, are infeoted also.The other receptor for HIV is a chemokine receptor such as CCR5. The NEF proteinis an important virulence factor. It reduces class I MHC protein synthesis, therebyreducing the ability of cytotoxic T cells to kill HIV-infected cells.Cytotoxic T cells are the main host defense against HIV.Laboratory Diagnosis: Virus can be isolated from blood or semen, but thisprocedure is not routinely available.Diagnosis is 'usually made by detecting antibody with ELISA as screening testand Western blot as confirmatory test.Determine the "viral load", ie, the amount of HIV in the plasma, using PCRbased assays. PCR-based assays can also detect viral RNA in infected cells, whichis useful to detect early infections.Treatment: Azidothymidine (AZT), 3TC, d4T, ddl, and ddC inhibit HIV18
replication by inhibiting reverse transcriptase. Protease inhibitors, eg, indinavir,prevent cleavage of precursor polypeptides.Highly active retroviral therapy (HAART) consists of two nucleoside inhibitorsand one protease inhibitor. Non-nucleoside inhibitors such as nevirapine are alsouseful.Clinical improvement occurs, but the virus persists. Treatment of theopportunistic infection depends on the organism.Prevention: Screening of blood prior to transfusion for the presence ofantibody."Safe sex," including the use of condoms. AZT with or without a proteaseinhibitor should be given to HIV-infected mothers and their newborns.AZT, 3TC, and a protease inhibitor should be given after a needle-stick injury.There is no vaccine.Hepatitis С VirusDisease: Hepatitis C; associated with hepatocellular carcinoma.Characteristics: Enveloped virus with one piece of single-stranded, positivepolarity RNA.No polymerase in virion. HCV has multiple serotypes.Transmission: Most transmission is via blood. Sexual transmission andtransmission from mother to child probably occurs as well.Pathogenesis: Hepatocellular injury probably caused by cytotoxic T cells.HCV does not cause a cytopathic effect.More than 50% of infections result in the chronic carrier state.The chronic carrier state predisposes to chronic hepatitis and to hepatocellularcarcinoma.Laboratory Diagnosis: Serologic testing detects antibody to HCV.Treatment: Alpha interferon mitigates chronic hepatitis but does not eradicatethe carrier staie.Prevention: Posttransfusion hepatitis can be prevented by detection ofantibodies in donated blood. There is no vaccine, and hyperimmune globulins are19
not available.Hepatitis D VirusDisease: Hepatitis D (delta).Characteristics: Defective virus that uses hepatitis В surface antigen as itsprotein coat. HDV can replicate only in cells already infected with HBV; ie, HBV isa helper virus for HDV.Genome is one piece of single-stranded, negative-polarity, circular RNA. Nopolymerase in virion.Transmission: Transmitted by blood, sexually, and from mothej; to child.Pathogenesis: Hepatocellular injury probably caused by cytotoxic T cells.Chronic hepatitis and chronic carrier state occur.Laboratory Diagnosis: Serologic testing detects either delta antigen orantibody to delta antigen.Treatment: Alpha interferon mitigates symptoms but does not eradicate thecarrier state.Prevention: Prevention of HBV infection by using the HBV vaccine and theHBV hyperimmune globulins will prevent HDV infection also.RNA NONENVELOPED VIRUSESPoliovirusDiseases: Paralytic poliomyelitis and aseptic meningitis.Characteristics: Naked nucleocapsid with single-stranded, positive-polarityRNA. No virion polymerase. There are three serotypes.Transmission: Fecal-oral route.Pathogenesis: The virus replicates in the pharynx and the gastrointestinaltract.It can spread to the local lymph nodes and then through the bloodstream to thecentral nervous system.20
Most infections are asymptomatic or very mild. Aseptic meningitis is morefrequent than paralytic polio.Paralysis is the result of death of motor neurons, especially anterior horn cells inthe spinal cord. Pathogenesis of postpolio syndrome is unknown.Laboratory Diagnosis: Recovery of the virus from spinal fluid indicatesinfection of the central nervous system.Isolation of the virus from stools indicates infection but not necessarily disease.It can be found in the gastrointestinal tract of asymptomatic carriers.The virus can be detected in cell culture by CPE and identified by neutralizationwith type-specific antiserum.A significant rise in antibody titer in convalescent-phase serum is alsodiagnostic.Treatment: No antiviral therapy is available.Prevention: Disease can be prevented by both the inactivated (Salk) vaccineand the attenuated (Sabin) vaccine; both induce humoral antibody that neutralizesthe virus in the bloodstream.The oral Sabin vaccine is used for routine childhood immunizations, because it(1) induces IgA immunity in the gut, thereby interfering with transmission;(2) induces immunity of longer duration; and(3) is administered orally.Current practice in the United States is to give two immunizations of the inactivated vaccine followed by the live, attenuated vaccine.The inactivated vaccine induces antibodies, which can prevent virulentrevertants in the live vaccine from causing paralytic poliomyelitis.Immune globulins are available but rarely used.CoxsackievirusesDiseases: Aseptic meningitis, herpangina, pleurodynia, myocarditis, andpericarditis are the most important diseases.Characteristics: Naked nucleocapsid with single-stranded, positive-polarityRNA. No virion polymerase.21
Group A and В viruses are defined by their different pathogenicity in mice.There are multiple serotypes in each group.Transmission: Fecal-oral route.Pathogenesis: The initial site of infection is the oropharynx, but the main siteis the gastrointestinal tract. The virus spreads through the bloodstream to variousorgans.Laboratory Diagnosis: The virus can be detected by CPE in cell culture andidentified by neutralization. A significant rise in antibody titer in convalescentphase serum is diagnostic.Treatment: No antiviral therapy is available.Prevention: No vaccine is available.Hepatitis A VirusDisease: Hepatitis A.Characteristics: Naked nucleocapsid virus with a single-stranded, positivepolarity RNA. No virion polymerase. Virus has a single serotype. (Fig. 6).RNACapsidFig. 6. Structure of Hepatitis A VirusTransmission: Fecal-oral route.Pathogenesis: The virus replicates in the gastrointestinal tract and thenspreads to the liver during a brief viremic period.22
The virus is not cytopathic for the hepatocyte. Hepatocellular injury is caused byimmune attack by cytotoxic T cells.Laboratory Diagnosis: The most useful test is IgM antibody.Isolation of the virus from clinical specimens is not done.Treatment: No antiviral drug is available.Prevention: Vaccine contains killed virus. Administration of immune globulinduring the incubation period can mitigate the disease.RotavirusDisease:Rotavirus causes gastroenteritis (diarrhea), especially in youngchildren.Characteristics: Naked double-layered capsid with 10 or 11 segments ofdouble-stranded RNA.RNA polymerase in virion. Rotavirus is resistant to stomach acid and hence canreach the small intestine. There are at least six serotypes.Transmission: Rotavirus is transmitted by the fecal-oral route.Pathogenesis: Rotavirus infection is limited to the gastrointestinal tract,especially the small intestine.Laboratory Diagnosis: Detection of rotaviras in the stool by ELISA.Isolation of the vir
The two major antigens are the hemagglutinin and the neuraminidase on separate surface spikes. Antigenic shift in these proteins as a result of re-assortment of RNA segments accounts for the epidemics of influenza caused by influenza A virus. Influenza A viruses of
Viruses have an inner core of nucleic acid surrounded by protein coat known as an envelope Most viruses range in sizes from 20 – 250 nm Viruses are inert (nucleoprotein ) filterable Agents Viruses are obligate intracellular parasites
of computer viruses. It thus appears that the concept of computer viruses is a novelty in scientific literature at this point, and that little effective protection against viruses is currently available. We begin the discussion of viruses with an informal discussion based on an English language definition.
Viruses are inert (nucleoprotein ) filterable Agents Viruses are obligate intracellular parasites Viruses cannot make energy or proteins independent of a host cell Viral genome are RNA or DNA but not both. Viruses have a naked capsid or envelope with attached proteins Viruses do
Interface in Simulink Azad Ghaffari San Diego State University Department of ECE San Diego CA 92182-1309 12/20/2012 This document provides a tutorial introduction to the dSPACE software (ControlDesk Next Generation version 4.2.1), the dSPACE DS1104 R&D controller board, and their use
III. Definition of a Virus 9 IV. Classification and Nomenclature of Viruses 13 V. Viruses of Other Kingdoms 20 VI. Summary 21 I. INTRODUCTION Plant viruses are widespread and economi-cally important plant pathogens. Virtually all plants that humans grow for food, feed, and fiber are affected by at least one virus. It is the
theory to viruses. Viruses defined as infectious sub cellular and ultra microscopic particles, whose transmission land replies causes reactions in the last cells. Viruses cannot be visible without the aid of electron microscope. Viruses lack the internal organization which is the characteristics of a cell.
Chapter 2 Virus, Bacteria, Protista, Fungi.notebook 1 April 19, 2018 Jan 21 2:32 PM complete petri dishes Chapter 2 Viruses, Bacteria, Protists, and Fungi Viruses Lesson 1 Objectives Name and describe the characteristics of viruses and how they multiply. Discuss both positive and negative ways that viruses
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