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VIRUS MORPHOLOGY:
Capsid: Composed of numerous repeating subunits. Viral genome is thus conserved in that a single protein can be
transcribed many times to make the capsid.
Capsomere: Clusters of polypeptides which, when completely assembled, form the capsid.
Nucleocapsid: Genome together with capsid.
Virion: Free viral particle, consisting of nucleocapsid, or nucleocapsid plus envelope.
Envelope: Lipid bilayer, usually obtained from host cell.
Symmetry: Three types
o Cubic Symmetry: Icosahedral symmetry. 20 equilateral triangles.
o Helical symmetry
o Complex: No regular symmetry, as in poxvirus.
Viral Conditions:
o Alkaline kills all viruses.
o Ether: Enveloped viruses are susceptible to ether. Poxviruses vary in susceptibility.
o Enveloped viruses are generally less stabile than naked viruses.
Host-cell Virus Interactions:
o Productive Infection: Virus successfully completes replication cycle and produces progeny virions.
o Abortive Infection: Virus enters the host-cell but cannot successfully complete replication.
Can result from a non-permissive host-cell, or because the virus is defective.
Abortive infections can become persistent infections.
o Restrictive Infection: Cells are only transiently permissive, after which they become non-permissive. This
results in transformation of the cell.
o Latent Infection: Virus remains in a cell and does not replicate, as in HSV, VZV, CMV, EBV, and HIV.
Replication Cycle:
o Divided according to presence of infectious virions:
Eclipse Phase: Virus has entered cell, but no progeny virions are created yet.
Maturation Phase: Viral progeny are produced and infectious virions are again present.
o According to biosynthesis sequence
Early Phase: Biosynthesis of prerequisite proteins, required before replication can take place, such as
replicase enzymes or enzymes that inhibit host-cell synthesis.
Late Phase: Synthesis of structural capsid proteins, and actual replication of the genome.
BASICS of REPLICATION:
(+)-STRAND RNA: The RNA genome can directly serve as an mRNA, because it contains its own 5' cap and 3' Poly-A
tail.
o Isolated mRNA strands are infectious.
(-)-STRAND RNA: They contain no cap and tail.
o Isolated mRNA strands are not infectious.
o They utilize a viral RNA-Dependent RNA-Polymerase to make (1) Subgenomic mRNA's (non-structural and
structural proteins), and (2) a complementary (+) RNA genome.
o The positive-strand RNA genome then serves as a template to make more minus-strand RNA's, to be packaged
with the structural proteins.
Polyproteins are often made by viruses, which are then cleaved, as eukaryotic machinery can't recognize a polycistronic
mRNA.
Double-Stranded DNA: Herpes, Papova, Adeno
o Early Genes are transcribed by host cell RNA-Polymerase, to form early proteins.
o These early proteins include a viral DNA-Dependent DNA Polymerase, which then forms progeny DNA.
o After replication, late genes are transcribed and translated, forming structural proteins.
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Diagnostic Techniques:
Direct Examination
o Light Microscopy
o Fluorescent Microscopy
Direct FA: Antigen plus patient's serum will produce antibody if patient's serum contains the
appropriate specific antibody.
Indirect FA: Antigen + antibody + anti-antibodies. It is cheaper and more commonly used.
o Electron Microscopy
Immune Electron Microscopy
o Solid Phase Immunoassay: Most common method today
RIA
ELISA
o Nucleic Acid Hybridization
Isolation and Identification
Serodiagnosis
o RIA: Detection of antigen.
o ELISA: Detection of antigen. Commonly done on HIV.
o Neutralization Test: Mix known virus with patient's serum, and if the patient's serum contains antibodies then
viral growth will be inhibited.
o Hemagglutinin Test:
INTERFERONS (IFN):
GENERAL PROPERTIES:
o Is secreted out of host cell, usually found in a dimer or multimeric form.
o IFN goes out, binds to specific receptors on neighboring cells, and changes their transcription in such a way as to
give them anti-viral properties.
o ds-RNA and LPS are both good inducers of IFN.
FUNCTION: Suggested mechanism of action involves RNA endonuclease activity, and induction of transcription of new
genes.
o IFN also prevents DNA synthesis and thus inhibits cell growth.
o ANTI-TUMOR: IFN's generally have some anti-tumor activity, particularly on leukemias and lymphomas. They
induce the production of HLA antigens on tumor cells, thereby allowing the immune system to recognize the
tumor cell.
RESISTANT: CMV and VZV are resistant to IFN. Other viruses are mostly susceptible.
INTERFERON-alpha: Produced by leukocytes.
o Receptor gene for IFN-alpha is on Chrom #21
o FNXN: Has been approved as a treatment for rare B-Cell Hairy Leukemia.
INTERFERON-beta: Produced by fibroblasts.
o Receptor gene for IFN-beta is on Chrom #21
INTERFERON-gamma: Produced by (1) unsensitized lymphoid cells, or (2) sensitized TH1 cells.
o It is stronger than other two in its antiviral properties.
o Receptor gene for IFN-gamma is on Chrom #6
ANTIVIRAL CHEMOTHERAPY:
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RIBAVIRIN:
o ACTION: Inhibits viral transcription, by binding to and inhibiting enzymes involved in nucleic acid metabolism.
Specifically inhibits inosine monodehydrogenase, involved in the synthesis of GTP.
o SIDE-EFFECTS: It is toxic in that it does not discriminate well between host cell and virus. Toxic to liver cells
and can cause anemia.
o VIRUSES: RSV in infants, and Lassa Fever intravenously.
ACYCLOVIR:
o ACTION: It is converted by HSV viral Thymidine Kinase into a monophosphate activated form. Host cell then
converts monophosphate form into triphosphate form. This form then does two things:
Binds and inhibits viral DNA polymerase
It is incorporated into viral DNA, where it acts as a chain-terminator.
o RESISTANCE in HSV is due to mutations in two different viral proteins:
Viral Thymidine Kinase, preventing conversion of acyclovir to the triphosphate form.
Viral DNA polymerase, such that it doesn't bind the drug.
o VIRUSES: Specific for HSV infections: HSV-1, HSV-2, VZV, but not CMV or EBV.
Resistance can occur, due to mutations in either Thymidine Kinase or viral DNA polymerase.
ADENINE ARABINOSIDE (Ara A):
o ACTION: Binds to DNA-Polymerase -- cellular or viral, thus bad side effects.
o VIRUSES: Used to be used for HSV-Encephalitis cases. Now surpassed by Acyclovir.
GANCICLOVIR:
o VIRUS: CMV, promising new treatment. Also works on HSV.
Up to 80% of HIV patients will relapse if therapy is discontinued. CMV pneumonia does not respond as
well as other CMV infections.
o ACTION: Nucleoside analog of guanosine, similar to Acyclovir.
o SIDE-EFFECTS: Reversible neutropenia, liver and CNS toxicity.
AZIDOTHYMIDINE (AZT, ZIDOVUDINE):
o ACTION: Inhibits Reverse Transcriptase.
AZT is phosphorylated first by host enzymes.
o VIRUS: HIV-1
Kuru
Creutzfeldt-Jacob Disease
Scrapie
Mad-Cow Disease
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DNA VIRUSES
PARVOVIRIDAE:
STRUCTURE: ds-DNA, circular. No envelope. Supercoiled double-stranded circles of DNA, wrapped around host
histones to form a chromosome-like structure.
HUMAN PAPILLOMAVIRUSES:
o PATHOGENESIS: Papillomavirus replicates in host nucleus but it does not integrate as a provirus.
Virus is species-specific, and it is tissue-specific to epithelial cells only.
o REPLICATION: Genome divided into Early region (early proteins) and late region (late proteins)
Early Proteins (E1-E8): Synthesized before DNA replication. The proteins are important in
replication, transcription, and oncogenic transformation.
Late Proteins (L1-L2): Synthesized after DNA replication. Structural proteins.
o DIAGNOSIS: Cytology, EM, or PCR. Does not grow well in culture.
o MANIFESTATIONS:
Common Warts (verruca): HPV-2,4 Thickening of the epidermis, and hyperkeratosis.
Terminally differentiated surface epithelial cells are permissive, so the virus multiplies in those
cells. These cells eventually die from lytic infection.
Basal Cells are non-permissive. Only the early genes are produced in these cells -- until they
differentiate to epithelial cells.
Gene products of the early genes stimulate differentiation of the basal cells and
growth of the wart.
Common in children. Lower incidence in adults may be because of acquired immunity.
Deep Plantar Warts: HPV-1,2
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HEPADNAVIRIDAE:
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Term
Abbrev
Description
HBsAg
Surface antigen present on viral envelope. Its presence indicates acute HBV
infection.
Anti-HBs
Antibodies to the surface antigen are not detectable during acute infection
even though they are being made, because there is way more antigen and it
sops it all up, making it undetectable in the blood.
Presence of Anti-HBs indicates immunity to HBV or previous vaccination
for HBV.
HBcAg
Anti-HBc
Hepatitis B e Antigen
HBeAg
This is the hepatitis viral polymerase and is present during acute infection.
Antibodies to Hepatitis-B e
Antigen.
Anti-HBe
These aren't usually tested but are present during acute or chronic infection.
Antibodies to Hepatitis-A
Anti-HAV
Antibodies to Hepatitis-C
Anti-HCV
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ADENOVIRIDAE:
STRUCTURE: ds-DNA, linear, non-enveloped, enclosed in a cubical capsid. Capsomeres form hexons and pentons.
REPLICATION: In nucleus.
o The DNA has an accessory protein covalently linked at the 5' end, which aids in viral replication.
o Early genes are transcribed in the cytoplasm. Early proteins inhibit host DNA synthesis and promote viral DNA
synthesis and late gene expression.
o Late genes transcribe a long mRNA that is differentially spliced to form structural proteins.
o Replication differs from SV40 virus in that it proceeds from the ends toward the center, but there are no Okazaki
fragments.
ADENOVIRUS: 41 serotypes, grouped A-G.
o PATHOGENESIS: Infects epithelial cells lining respiratory tract, GI tract, and conjunctiva.
It persists in lymphoid tissues such as Peyer's Patches may be reactivated in immunosuppression.
Produces a cytopathic effect (CPE) of grape-like clusters in culture.
o TRANSMISSION: Fecal-oral, respiratory.
o MANIFESTATIONS: Only a small number of infections.
Acute Respiratory Infections: Types 4-7. Military recruits now get a vaccine to prevent this.
Conjunctivitis: Types 3 and 8. Epidemic keratoconjunctivitis or Shipyard-Eye.
Acute Gastroenteritis: Types 40 and 41, especially in infants.
Acute Hemorrhagic Cystitis: Young males; types 11 and 22.
Cervicitis and urethritis: Types 37
Pharyngoconjunctival fever: In children, types 3 and 7
Acute febrile pharyngitis
HERPESVIRIDAE:
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RNA VIRUSES
PICORNAVIRIDAE:
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STRUCTURE: Smallest of RNA viruses, ss (+) RNA, non-enveloped, linear, infectious. No cap but there is a viral
protein linked to the 5' end.
o Rigid capsule makes fecal-oral transmission possible
o A large number of infectious viral particles is produced. Humoral immunity is crucial to fighting these.
o Non-enveloped structure makes it a good GI pathogen, able to survive in GI tract.
REPLICATION: Cytoplasmic, RNA-Dependent RNA Polymerase.
o Entire genome is immediately translated into a polyprotein.
o Polyprotein is cleaved into several small constituents:
Viral RNA-Dependent RNA Polymerase
Structural proteins
o RNA Dependent RNA Polymerase then makes a minus-strand RNA out of the plus-strand RNA.
o The minus-strand RNA is then used as a template for making additional (plus-strand) viral particles.
ENTEROVIRUSES:
o CONDITIONS:
Stable at pH 3, thus it can replicate in stomach.
Optimal temp is 37C, favoring GI tract.
o EPIDEMIOLOGY: Highly communicable. Fecal-oral transmission, respiratory, person-to-person.
Peak occurrence in summer and fall.
Incubation period of 3-5 days for localized infections, or longer for generalized illnesses.
Virus is tropic for lymphoid tissue in small intestine and pharynx.
o General Manifestations: Usually asymptomatic or associated with mild illness. Even though GI tract is a major
site of replication, GI symptoms are rarely seen (except as a consequence of generalized illness).
o IMMUNITY: Acquired immunity is lifelong and serotype specific. Humoral and mucosal immunity is important,
to counteract free viral particles.
Enteroviruses that infect the gut produce a good IgA response, whereas viruses that infect only the
upper respiratory tract do not produce as good a response.
o POLIOVIRUS:
STRUCTURE: 3 serotypes.
Ig-Superfamily cell-surface receptor protein has been identified.
DIAGNOSIS:
MANIFESTATIONS: Only 1 in 200 infections come down with Paralytic Poliomyelitis.
Infection of anterior horn cells of spinal cord (spinal poliomyelitis) or pontine nuclei (bulbar
poliomyelitis).
Symptoms: Myalgia, generalized weakness, followed by flaccid paralysis.
Post-Polio Syndrome (PPS): Strange symptoms, thought to be due to nerve cell attrition, very
late in the course of disease. Fatigue, muscle weakness, and respiratory difficulty.
VACCINE: Sabin (live, oral) and Salk (dead). Most remaining cases of Polio today are residuals of the
live attenuated vaccine.
The Sabin Oral Polio vaccine should not be given to people with HIV. Other live vaccines
(measles, mumps, HBV, influenza) can be given.
Enhanced Polio Inactivated Vaccine has been developed recently. Will be given as the first
shot -- inactivated vaccine, in order to prevent patient from getting polio from vaccine.
Subsequent booster shots will then be the oral polio vaccine.
o COXSACKIEVIRUSES:
COXSACKIEVIRUS A: 26 serotypes.
MANIFESTATIONS: Usually just mild respiratory disease.
ASEPTIC MENINGITIS:
Viral Meningitis occurs in Summer and Fall -- not Winter and Spring as in
Mumps virus.
Coxsackie A&B, and Echovirus account for 80-90% of all cases of viral
aseptic meningitis.
Important to distinguish it with partially treated bacterial meningitis:
lumbar puncture will show lymphocytes (not PMN's), and a normal glucose
(not low glucose).
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STRUCTURE: ss (+) RNA, lipid envelope, "crown-like," more than twice as large as Picornaviridae.
DIAGNOSIS: It isn't cultured, but must distinguish it from bacterial otitis media or pharyngitis. Culture for Strep-A.
IMMUNITY: Acquired immunity is poor; reinfection with same strain occurs.
MANIFESTATIONS:
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CALICIVIRIDAE:
RETROVIRIDAE:
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STRUCTURE: ss (+) RNA, cap and tail, diploid (two copies), enveloped.
o The two copies of RNA are base-paired to each other, and are hooked to an accessory tRNA which is essential
for replication.
o Reverse Transcriptase: RNA-Dependent DNA Polymerase. It is encoded by Pol gene and has three different
functions.
RNA-Dependent DNA Polymerase (make ds-DNA out of RNA)
RNAse-H: This activity degrades the RNA portion of the RNA:DNA hybrid during replication.
Located on the same protein as the RT action.
Integrase: This activity cleaves host and viral DNA in preparation for integration of virus into host
genome. Separate protein cleaved from the pol transcript.
o Long Terminal Repeats (LTR'S): Genome contains LTR's at each end, which have some sequences in them
unique to each virus.
R: Redundant sequences at both ends of genome.
U5: Unique sequence at 5' end.
U3: Unique sequence at 3' end.
o THREE RETROVIRAL GENES: These genes are required by all retroviruses for successful replication.
Gag: Group-Antigen. Encodes a structural precursor protein.
Pol: Polymerase. Encodes the Reverse Transcriptase.
Env: Envelope-protein. Encodes glycoproteins that become a part of the viral envelope.
ONCOVIRUS PARTICLES: Retroviruses become proviruses and can cause transformation by several mechanisms. They
can induce host-genome mutation (insertional mutagenesis), and they can act as transposable elements.
o Four major types recognized.
A-Type: Non-infectious
B-Type: Budding through plasma membrane with eccentric core. MMTV.
C-Type: Most Common. Budding through plasma membrane with central core. Includes HTLV, RSV
(Rous-Sarcoma), MuV.
D-Type: Some primate viruses.
o Two Categories:
Acute: v-onc+ viruses have genes homologous to host proto-oncogenes. They are defective in that they
can't replicate -- replication-deficient transformation-competent v-onc+ viruses.
Chronic: Not in themselves v-onc+ genes, but rather they cause transformation long after infection by
insertional mutagenesis. Usually cause leukemia.
o Specific Viral Oncogenes: v-onc genes.
arc: Role in Rous Sarcoma. It encodes a Tyrosine Kinase.
erbB: Encodes a receptor for Epidermal Growth Factor (EGF-R).
sis: Encodes PDGF.
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ras: Encodes GTPase activity. v-ras (oncogene) differs from c-ras (protooncogene) by one codon.
myc: In Burkitt's Lymphoma, it is involved with an Ig gene in a 8:14 translocation.
abl: Involved in 9:22 translocation with bcr to form the Philadelphia chromosome, in Chronic
Myelocytic Leukemia (CML).
erbA: A thyroid-hormone receptor in birds. It blocks the differentiation of proliferating erythroid
precursor cells.
o Tumor-Suppressor Genes:
Retinoblastoma (Rb) Gene:
Wilms Tumor Gene:
p53:
REPLICATION: Via reverse transcriptase
o Cytoplasmic Stage: Particle is not immediately uncoated. RNA genome utilizes Reverse Transcriptase to make
a double-stranded copy of DNA (RNA ------> cDNA ------> dsDNA). Then the RNA is degraded.
It utilizes a hydrogen-bonded host-cell tRNA as a primer.
o Nuclear Stage: ds-DNA copy enters nucleus. It becomes integrated as a provirus, with the aid of the nuclease
activity of Reverse Transcriptase. If integration fails, then the virus can't survive. Thus it's a potential drug target.
Transcription then ensues and viral mRNA is made. The unspliced transcripts serve as progeny genome.
Gag, Pol, and Env proteins are translated, glycosylated, and incorporated with the genome as a new
virion particle is formed.
Endogenous Proviruses: Human have a few silent endogenous proviruses: EREV1, and ERV3. They are both defective
and produce no symptoms.
HUMAN T-LYMPHOMA VIRUS (HTLV-1): (ONCOVIRINAE)
o STRUCTURE: Type-C Oncovirus particle.
o MANIFESTATIONS: Adult T-Cell Leukemia / Lymphoma (ATL). The virus infects CD4+ T-Cells, causing
proliferation.
tax/rex gene is the single viral gene that is implicated in oncogenesis. HTLV virus is integrated into the
infected cell as a provirus (no replication occurs). The mechanism of transformation is unknown, but
they think it is acute and that the virus has v-onc+ genes.
Symptoms: Skin manifestations, hypercalcemia, leukocytosis, hepatosplenomegaly.
Bad prognosis.
Rous Sarcoma Virus (RSV): (Oncovirinae). Causes sarcoma in birds.
HUMAN IMMUNODEFICIENCY VIRUS (HIV): (LENTIVIRINAE)
o SUBTYPES:
HIV-1: Human HIV.
HIV-2: More closely related to SIV and infects monkeys.
o STRUCTURE:
Gag, Pol, and Env proteins.
Accessory Proteins:
vpu protein is required for maturation and budding.
tat (transactivator of transcription): Activates transcription of the major viral mRNA's.
Glycoproteins: Encoded by the Env genes. gp160 is the precursor glycoprotein, which is then cut in
two:
gp120: Also called the 'Secretory Subunit." High antigenic variability.
High degree of antigenic shift. We make antibodies to gp120, but it is always
changing its antigenic specificity.
Has V1-V5 Variable Regions. V3 is responsible for M-Tropism. The CD4
binding domain lies in between V4 and V5.
It is responsible for the binding of the virus to CD4+ receptors.
gp41: Transmembrane component. Less antigenic variability.
Responsible for the fusion of viral and cell membranes.
Also confers the tropism on the cell -- L-Tropic or M-Tropic.
Protease Inhibitors inhibit this cleavage.
Structural Proteins: Capsid proteins encoded by the Gag gene.
P55 is cleaved by protease into 5 substituents, including P24.
These structural proteins are required for viral replication.
Protease Inhibitors inhibit this cleavage.
o VIRUS-TROPISM: Conferred by gp41 glycoprotein.
L-Tropic: Attracted to lymphocytes (CD4+ cells)
Infection of TH cells accounts for depressed CD4 count.
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Neuraminidase (NA) is released from infected cells. Another source of antigenic types.
There are 9 subtypes of NA. Only N1, N2 are found in humans.
REPLICATION: In host nucleus. Cap-snatching transcription. Viral RNA's utilize portions of host-cell RNA to make
their own 5' Cap in the host cell nucleus.
ANTIGENIC VARIATION:
o Antigenic Shift: Major source of antigenic variation, due to re-assortment of the RNA genome segments. It leads
to changes of subtype of the envelope glycoproteins.
o Antigenic Drift: Minor changes in antigenic variation, due to point mutations in the genome.
INFLUENZA VIRUS-A: 8 segments.
o DISTRIBUTION: Found in humans, aquatic birds, swine, horses, seals, whales.
o EPIDEMIOLOGY: This is the major player in flu epidemics, because of its antigenic variation. Highly
contagious, spread by person-to-person contact.
o MANIFESTATIONS: It targets the epithelial cells of the respiratory tract, upper and lower.
Epithelial cells become ciliastatic as a result of infection, which can predispose to more serious
bacterial infections.
Incubation Period: 1-4 days.
Symptoms: Soar throat, fever, chills, myalgia, headache.
Normally Self-Limiting infection, lasting 3-7 days. Cough may last 1-2 weeks.
INFLUENZA VIRUS-B: 8 segments
o DISTRIBUTION: Found only in humans
o EPIDEMIOLOGY: Less serious infection than Type-A. Generally found in children or adolescents.
o Influenza-B does not undergo reassortments or antigenic shift.
INFLUENZA VIRUS-C: 7 segments.
o DISTRIBUTION: Found in humans and swine.
o EPIDEMIOLOGY: Rarely causes diseases. Ubiquitous, and we all generally have antibodies by early childhood.
INFLUENZA VACCINE: Constantly updated, as CDC keeps track of antigenic types of latest strains.
o In the past they've used inactivated whole viruses.
o This year they are using a trivalent subunit vaccine consisting of purified viral HA antigen: (1) Type-A H1N1
and (2) H3N2, and Type-B antigen.
o Vaccine administered during the fall. Breakouts are in winter.
o
PARAMYXOVIRIDAE:
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o Primary transcription ------> genome replication ------> more transcription and translation occur post-replication.
o Nucleocapsids bud through host cell-membrane to form new particles.
EPIDEMIOLOGY:
o Racoons are the most common animal carrier today.
o Bats are most common carrier in U.S. to actually result in infection.
o Also skunks, wild mammals, and unvaccinated domestic mammals.
DIAGNOSIS: Look for Negri bodies in the animal tissue.
MANIFESTATIONS:
o PATHOGENESIS:
Virus replicates in striated muscle at site of bite. Then it travels up nerve endings to spinal cord and
brain.
Virus hooks to Acetylcholine receptors at neuromuscular junction.
o Symptoms: Fatal encephalitis. Hypertonic muscle contraction, convulsions, coma, death.
Hydrophobia happens as swallowing would precipitate a spasm of throat muscles.
TREATMENT: No treatment known.
o PREVENTION: Post-exposure immunization, both passive and active, should be given prophylactically in
cases of possible infection.
Human Rabies Immune Globulin (HRIG) administered on same day as first vaccine dose, but at a
different site.
Human Diploid Cell Vaccine (HDCV) is the new active vaccine (inactivated virus), grown in human
diploid fibroblast cells. Given in 6 doses.
VESICULAR STOMATITIS VIRUS (VSV): Arbovirus causes disease in cattle and horses. Can cause mild disease in
humans. Has been utilized as a model virus in research.
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STRUCTURE: Non-enveloped, double-stranded segmented (-) RNA, in 10-12 segments. Contains concentric inner and
outer capsids.
o VP4: Viral glycoprotein neutralization antigen.
o VP7: Viral glycoprotein neutralization antigen, derived from host-cell ER.
o RNA-dependent RNA-Polymerase can make messenger RNA's out of the double-stranded viral genome.
o Rigid capsule makes fecal-oral transmission possible.
REPLICATION: The inner capsid always remains intact.
o The outer capsid is removed upon entry into the cell.
o Inside the capsid, the RNA-dependent RNA-polymerase makes subgenomic (+) mRNA's. These mRNA's are
transported into host-cell cytoplasm and translated into proteins.
o Inside the capsid, the (-) RNA's are used as templates to make new ds-RNA genomes, which are then released
outside the capsid.
o The new genomes are assembled along with the viral proteins to make new infectious particles.
EPIDEMIOLOGY: Fecal-oral transmission.
o Infection occurs in 6 months to 2 years old. Neonates, older children, and adults are usually asymptomatic.
Breast-milk IgA probably provides protection for neonates.
o Prevalent in winter, but throughout year in tropical climates. Unexplained west-to-east trend in seen in its
incidence: Nov ------> Feb as you go from West ------> East in United States.
REOVIRUS: (ORTHOREOVIRUS)
o STRUCTURE: 3 serotypes.
o MANIFESTATIONS: Commonly infects, but asymptomatic, hence they are orphan viruses.
ROTAVIRUS: Group-A Rotavirus has 4 serotypes, based on the VP7 antigen.
o MANIFESTATIONS: Gastroenteritis, which can be life threatening. It is the major cause worldwide, in infants
and young children.
MECH is believed to be decreased absorption at brush border, but not sure.
o IMMUNITY: Serotype-specific, and incomplete.
o DIAGNOSIS: ELISA of stool samples
o TREATMENT: IV-fluid replacement. Oral rehydration therapy.
o VACCINE: In clinical trials are re-assortment-viruses containing genomes that encode VP4 or VP7. These are
human viruses that infect the cell and reassort with the segmented genome of the rotavirus, rendering it nonpathogenic.
ORBIVIRUS: All are arboviruses. Most are asymptomatic. 10 segments.
o COLORADO TICK FEVER VIRUS:
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MANIFESTATIONS: Standard common viremia symptoms: fever, myalgia, rash, vomiting. May see
maculopapular rash.
STRUCTURE: Has 12 segments, not 10.
TOGAVIRIDAE:
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FLAVIVIRIDAE:
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STRUCTURE: ss (-) RNA, segmented, 3 segments. Enveloped. Spherical, helical nucleocapsid. There may be some
ambisense (+/-) characteristics.
o RNA-Dependent RNA-Polymerase is present.
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FILOVIRIDAE:
ARENAVIRIDAE:
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