micro_mod5_ms1

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soren101
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micro_mod5_ms1
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2011-08-02 17:23:17
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microbiology virology mod5 ms1
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virology mod5 ms1
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  1. DNA ICOSAHEDRAL NAKED VIRUS FAMILIES
    • PARVOVIRIDAE 18-26
    • POLYOMAVIRIDAE 45
    • PAPILLOMAVIRIDAE 55
    • ADENOVIRIDAE 70-90
  2. DNA ICOSAHEDRAL ENVELOPED VIRUS FAMILIES
    • HERPESVIRIDAE 110-200
    • HEPADNAVIRIDAE 42
    • IRIDOVIRIDAE 125-300
  3. DNA COMPLEX VIRUS FAMILIES
    POXVIRIDAE 100 x 240 x 300
  4. RNA ICOSAHEDRAL NAKED VIRUS FAMILIES
    • PICORNAVIRIDAE 20-30
    • CALICIVIRIDAE 35-40
    • ASTROVIRIDAE 28-30
    • REOVIRIDAE 60-80
    • BIRNAVIRIDAE 60
  5. RNA ICOSAHEDRAL ENVELOPED VIRUS FAMILIES
    • TOGAVIRIDAE 45-75 (RUBELLA - HELICAL)
    • FLAVIVIRIDAE 30-40
  6. RNA HELICAL ENVELOPED VIRUS FAMILIES
    • ARENAVIRIDAE 50-300
    • BUNYAVIRIDAE 90-100
    • CORONAVIRIDAE 80-160
    • RETROVIRIDAE 100-120
    • ORTHOMYXOVIRIDAE 80-120
    • PARAMYXOVIRIDAE 150-300
    • BORNAVIRIDAE ---
    • RHABDOVIRIDAE 75-180
    • FILOVIRIDAE (VARIABLE)
  7. ORTHOMYXOVIRUSES
    INFLUENZA VIRUSES

    (-)ssRNA

    8 SEGMENTS OF RNA & ENVELOPED

    ENTRY - HEMAGGLUTININ (HA) AND NEURAMINADASE (N) ADSORBS TO CELL GLYCOPROTEIN RECEPTORS VIA SAILIC ACID MOLECULES

    UNCOATING - ENDOCYTOSIS AND ENDOSOME ACIDIFICATION (PUMPS PROTONS THROUGH M2 CHANNEL; BLOCKED BY AMANTADINE & RIMANTADINE). VIRAL RNA INVADES NUCLEUS.

    TRANSCRIPTION - ERROR PRONE VIRAL RNA DEPENDENT RNA POL (RdRP) PRIMES SEGMENTS TO MAKE mRNA

    TRANSLATION - IN CYTOPLASM

    REPLICATION - BLAH

    ASSEMBLY - GENE SEGMENTS AND PROTS ASSEMBLE INTO PARTICLES AND GET HA & N BY BUDDING FROM PM
  8. PARAMYXOVIRUSES
    RESPIRATORY SYNCYTIAL, PAPRAINFLUENZA, MEASLES, MUMPS, METAPNEUMO, NIPAH, HENDRA

    (-)ssRNA

    NON-SEGMENTED & ENVELOPED

    ENTRY - FUSION WITH PM. NO RECEPTOR MEDIATED ENDO.

    UNCOATING - GENOME INJECTED INTO CYTOPLASM BY PM FUSION. NO NUCLEAR TRANSLOCATION.

    TRANSCRIPTION - RdRP PRIMES TRANSCRIPTION TO MAKE mRNA.

    TRANSLATION - BLAH

    REPLICATION - BLAH

    ASSEMBLY - ACQUIRE ENVELOPE BY BUDDING FROM PM
  9. CORONAVIRUSES
    COMMON COLD, SARS

    (+)ssRNA, NONSEG, ENV, HELICAL

    • HCoV-OC43 (URT & CNS)
    • HCoV-229E (URT)
    • HCoV-SARS (LRT - ERROR-PRONE)

    ENTRY - ACE II TO PM LEADS TO INJECTION OF GENOME INTO CYTOPLASM

    TRANSLATION - PART OF GENOME TRANSLATED TO MAKE 1 LONG POLYPEPTIDE. VIRAL PROTEASES CLEAVE TO MAKE RdRP.

    REPLICATION - TEMPLATE JUMPING; ERROR-PRONE

    ASSEMBLY - ON ENDOPLASMIC RETICULUM GOLGI INTERMEDIATE COMPARTMENT (ERGIC)

    BUDDING - FROM ERGIC THEN PASSES THROUGH PM

    • STRUCTURAL PROTS:
    • E - ENV
    • M - MATRIX OR MEMBRANE
    • S - SPIKE
    • N - NUCLEOCAPSID

    • NON-STRUCTURAL PROTS:
    • RdRP - Nsp12 & 9
    • PROTEASE - Nsp1, 2, & 5

    • OTHER VIRUSES:
    • FLAVI
    • TOGA
    • CALICI
    • ASTRO
  10. VIRUSES WITH 2 RNA GENOMES
    RETROVIRUSES (HIV & HUMAN T-LYMPHOTROPIC VIRUS)

    LTRs ACT AS PROMOTERS

    • PROTEINS:
    • GAG PRECURSOR - STRUCT PROTS, MATRIX (MA), CAPSID (CA), AND NUCLEOCAPSID (NC) PROTS. VIRAL PROTEASE (PR).

    POL PRECURSOR - REVERSE TRANSCRIPTASE (RT) AND INTEGRASE (IN).

    ENV PRECURSOR - REQUIRED FOR CELL ENTRY. SURFACE (SU aka gp120) AND TRANSMEMBRANE (TM aka gp41).
  11. HIV LIFE-CYCLE
    2 RNA GENOMES (LENTI)

    ENTRY - ENV PROT gp120 ATTACHES TO CD4 RECEPTOR. CO-RECEPTORS CXCR4 IN T-CELLS AND CCR5 IN MACROPHAGES. gp41 THEN MEDIATES FUSION (NO ENDOCYTOSIS).

    REVERSE TRANSCRIPTION - RT FROM VIRUS MAKES cDNA IN CYTOPLASM.

    DNA TRANSPORT - VIRAL Vpr PROT TAKES DNA TO NUCLEUS.

    DNA INTEGRATION - RANDOMLY INTEGRATED BY (IN)

    TRANSACTIVATION - CELLULAR RNA POL II BINDS TO LTR TO MAKE VIRAL RNA.

    RNA EXPORT - Rev PROT TAKES RNA TO CYTOPLASM.

    TRANSLATION - BLAH, THEN POLYPEPTIDE CLEAVED BY PR.

    ASSEMBLY - Vpu REQUIRED TO BRING COMPONENTS TO PM.

    BUDDING - BLAH
  12. LENTIVIRUS (HIV) ACCESSORY PROTEINS
    Vif - INH CELLULAR DEFENCE APPARATUS AGAINST INFECTION

    Vpr - TAKES GENOME TO NUCLEUS

    Tat - LTR TRANSACTIVATION

    Rev - TAKES mRNA FROM NUCLEUS TO CYTOPLASM

    Nef - IMMUNE EVASION BY DOWN REGULATING EXPRESSION OF MHC I

    Vpu - VIRUS ASSEMBLY
  13. HERPES LYTIC INFECTION
    ATTACHMENT TO CELL-SURFACE GLYCOPROTEINS AND FUSION WITH PM

    UNCOATING IN CYTOPLASM AND TRANSLOCATION OF GENOME AND PROTS TO NUCLEUS.

    DNA CIRCULARIZES, FOLLOWED BY TRANSCRIPTION.

    CELLULAR RNA POL II MAKES IMMEDIATE EARLY (IE - ALPHA) GENES --> ALPHA PROTS MADE IN CYTOPLASM.

    IE PROTS MOVE TO NUCLEUS TO TRANSACTIVATE EARLY (BETA) mRNA --> PROTS.

    INTRACELLULAR MOVEMENT OF VIRAL PROTS BASED ON THEIR STRUCTURE/FUNCTION.

    VIRAL DNA MAKES COPIES OF GENOME IN NUCLEUS.

    CELLULAR RNA POL II MAKES LATE (GAMMA) mRNA.

    REPLICATED DNA CLEAVED TO GENOME LENGTH FOR CAPSID. NUCLEAR BUDDING AFTER NUCLEOCAPSID, TEGUMENT, AND ENV ACQUIRED.

    ENV PARTICLES MAY UNDERGO DE-ENV RE-ENV STEPS BEFORE BUDDING.

    BUDDING
  14. ADENOVIRUS LIFE-CYCLE
    NON-ENV LINEAR dsDNA

    ENTRY - VIA ENDOSOME. CLATHRIN COATED VESICLES. VIRAL FIBER AND PENTON PROTS BIND WITH CELLULAR CAR & INTEGRINS.

    RELEASE - ACIDIFICATION CAUSES PATIAL LOSS OF CAPSID STRUCT. MOVES TO NUCLEUS VIA MICROTUBULES & DNA RELEASED INTO NUC.

    IMMEDIATE EARLY PROTS - CELLULAR RNA POL II MAKES IE E1A mRNA --> E1A PROTS MADE IN CYTO THEN MOVED TO NUC.

    EARLY PROTS - IN NUC, E1A PROMOTES EXPRESSION OF EARLY PROTS WHICH TOGETHER PROMOTE DNA REPLICATION.

    LATE PROTS - E1A AND EARLY PROTS PROMOTE EXPRESSION OF LATE PROTS FOR CAPSID.

    ASSEMBLY - DNA INSERTED INTO CAPSID.

    RELEASE - LYSIS
  15. PARAMYXOVIRUS STRUCTURE (PIC)
  16. PARAMYXOVIRUS CYCLE (PIC)
  17. CORONOVIRUS (PIC)
  18. CORONAVIRUS LIFE-CYCLE (PIC)
  19. HIV CYCLE (PIC)
  20. HERPESVIRUS (PIC)
  21. HERPESVIRUS LIFE-CYCLE (PIC)
  22. ADENOVIRUS LIFE-CYCLE (PIC)
  23. HPV (PIC)
  24. (-)ssRNA VIRUS SUMMARY
  25. (+)ssRNA VIRUS SUMMARY
  26. VIRUSES WITH 2 RNA GENOMES SUMMARY (PIC)
  27. DNA VIRUS SUMMARY (PIC)
  28. RHINOVIRUS
    PICORNA (+)ssRNA; NON-ENV; ICOSA

    URT

    ENDOCYTOSIS; LYSIS

    VP1,2,3 ATTACH TO ICAM1

    100+ SEROTYPES

    NO VIREMIA

    COMMON COLD; CROUP

    WINTER
  29. INFLUENZA A
    ORTHOMYXO

    (-)ssRNA; 8 SEGS;ENV; HELICAL

    REPLICATES IN NUC

    SIALIC ACID RECEPTORS

    ANI & HUM RESIVOIRS (SHIFT & DRIFT)

    HA & N; NO F

    NO VIREMIA

    AVEOLAR EDEMA, PNEUMONIA

    FEVER - IL-1 AND TNF-a
  30. INFLUENZA B
    ORTHOMYXO

    (-)ssRNA; 7 SEGS; ENV; HELICAL

    DRIFT; NO SHIFT
  31. AMANTADINE & RIMANTADINE
    INFLUENZA

    BLOCKS FLUVA M2
  32. OSELTAMIVIR & ZANAMIVIR
    INFLUENZA

    BLOCKS FLUVA AND FLUVB N

    BLOCKS CLEAVAGE OF SIALIC ACID SO VIRIONS CANNOT ESCAPE
  33. MEASLES (RUBEOLA)
    PARAMYXO

    (-)ssRNA; ENV; HELICAL

    HA & F; NO N

    VIREMIA; KOPLIK SPOTS; MACULOPAPULAR RASH (ENDOTHEL CELL KILLING)

    GIANT CELLS

    SUB-SCLEROSING PANENCEPHALITIS (CMI ON NEURONS)

    BLOCKS IFN INDUCED JAK/STAT

    PRIMARY MUCOSA --> SECONDARY LYMPH
  34. RSV
    PARAMYXO

    (-)ssRNA; ENV; HELICAL

    F ONLY

    MOST COMMON INFANT/CHILD VIRAL INFECTION


    NO VIREMIA
  35. PALIVIZUMAB/SYNAGIS
    TREAT RSV - BLOCK F PROTEIN

    FOR HIGH-RISK INFANTS, GIVE AERO RIBAVIRIN

    FLUORESCENT Ab
  36. PARAINFLUENZA
    PARAMYXO

    (-)ssRNA; ENV; HELICAL

    HA, N, F

    4 SEROTYPES: 1-3 PATHOGENIC

    URT IN ADULTS

    U/LRT IN KIDS: CROUP; TYPE 3 CAUSES SEVERE LRT & PULMONARY DISTRESS SYNDROME

    NO VIREMIA
  37. MUMPS
    PARAMYXO

    (-)ssRNA; ENV; HELICAL

    HA, N, F

    PARATITIS; ORCHITIS

    VIREMIA

    ASEPTIC MENINGITIS, MYOCARDITIS
  38. POLIO
    PICORNA - ENTERO

    (+)ssRNA; NON-ENV; ICOSA

    FECAL-ORAL; LYSIS; CPE

    LYMPH AND NERVOUS SYSTEM (MOTOR)

    ABORTIVE, NON-PATALYTIC, PARALYTIC
  39. TREAT POLIO
    VACCINES:

    eINTRAMUSCULAR - INACTIVATED, 3 SEROTYPES. NO IgA SO POOR GUT PROTECTION
  40. NOROVIRUS
    CALICI - ENTERO

    (+)ssRNA; NON-ENV; ICOSA

    90% OF EPIDEMIC NON-BAC GASTROENTERITIS

    FECAL-ORAL; CRUISE, NURSING

    >5 SEROTYPES; II MOST COMMON

    SAPOVIRUS ANOTHER CALICI
  41. ROTAVIRUS
    REO - ENTERO

    dsRNA; 11 SEGS, NON-ENV; DOUBLE-LAYERED CAPSID

    ENTRY THROUGH b-ADREN RECEPTORS

    6 SEROTYPES ABCDEF (A IN WINTER); LYSIS

    HA USED AS Ab

    MAJOR GI INFECTION IN INFANTS & CHILDREN

    DUAD TIPS - DEHYDRATION

    NSP4 - ENTEROTOXIN
  42. TREAT ROTAVIRUS
    ROTA-TEQ LIVE ORAL AGAINST 5 SEROTYPES

    ROTA-SHIELD -- LIVE VACCINE

    DETECTION IN STOOL; ELISA
  43. OTHER ENTEROVIRUSES
    ADENO 40 & 41: dsDNA; NON-ENV; ICOSO

    ASTRO: (+)ssRNA; NON-ENV; SIMILAR TO PICORNA AND CALICI

    ENT 70 - ACUTE HEM CONJUNCTIVITIS

    ENT 71 - MENINGITIS AND ENCEPH

    ENT 72 - SAME AS HEP A (PICORNA - (+)ssRNA, NON-ENV, ICOSO)
  44. COXSACKIE
    PICORNA - ENTERO

    (+)ssRNA; NON-ENV; ICOSO

    30+ SEROTYPES

    • GROUP A - HERPANGIA, ACUTE HEMORRHAGIC CONJUNCTIVITIS,
    • HAND-FOOT-AND-MOUTH

    • -GROUP B - PLEURODYNIA, MYOCARDITIS,
    • CONGESTIVE HEART FAILURE, AND PERICARDITIS (AFFECTS LIVER, HEART, PLEURA, PANCREAS)

    -BOTH GROUPS CAUSE URT DISEASE, FEBRILE RASHES, ASEPTIC MENINGITIS
  45. LIVER FUNCTION TESTS
    ALANINE TRANSAMINASE (ALT) - HEPATOCYTE ENZ PRESENT IN LIVER DAMAGE

    ASP TRANSAMINASE (AST) - ACUTE LIVER DAMAGE BUT LOCATED IN OTHER TISSUES SO NOT SPECIFIC TO LIVER

    ALANINE PHOS (ALP) - ALL TISSUES BUT CONC IN LIVER, USED TO DETECT BILE DUCT OBSTRUCTION, etc

    GAMMA GLUT TRANS (GGT) - RECENT ALC ABUSE, MINOR LIVER DYSFUNCTION
  46. HEP A
    PICORNA (+)ssRNA NON-ENV

    -ONE SEROTYPE

    -TRANSMITTED VIA FECAL-ORAL ROUTE

    -HUMANS ARE ONLY RESERVOIR

    APPEARS IN FECES 2 WEEKS BEFORE SYMPTOMS

    • -CHILDREN MOST FREQUENTLY
    • INFECTED (SUMMER CAMPS, BOARDING SCHOOL…)

    -RARELY TRANSMITTED VIA BLOOD BECAUSE VIREMIA IS LOW AND NO CHRONIC INFECTION

    -DIAGNOSE W/ IgM AB TITER; CAN ALSO ISOLATE THE VIRUS IN CELL CULTURE

    -NO ANTI-VIRAL THERAPY; ACTIVE IMMUNIZATION W/ VACCINE CONTAINING INACTIVATED HAV IS AVAILABLE

    -OR PASSIVE IMMUNIZATION: IMMUNE SERUM GLOBULIN CAN BE GIVEN WITHIN 14 DAYS OF EXPOSURE
  47. HEP B
    HEPADINOVIRUS

    PARTIALLY dsDNA; ENV; ICOSA

    MANY ASYMPTOMATIC, BUT ONCE ACTIVE MORE SEVERE THAT HEP A

    • -CONTAINS DNA-DEPENDENT DNA POLYMERASE; SYNTHESIZES MISSING
    • PORTION OF DNA

    DANE PARTICLES

    • SOME DNA INTEGRATES INTO HOST
    • GENOME

    -REPLICATION OCCURS IN NUCLEUS

    -CELLS RELEASED BY BUDDING

    -4 GENES: POL, ENV, PRE-CORE, AND X

    • -MALIGNANCY: HIGH INCIDENCE OF
    • HEPATOCELLULAR CARCINOMA (HEPATOMA)

    • -PRODUCES VIRIONS, SPHERES, AND
    • FILAMENTS (EMPTY ENVELOPES)

    • -CORE ANTIGEN FORMS CAPSID CORE OF
    • VIRION, E ANTIGEN IS SECRETED FROM INFECTED CELLS INTO BLOOD (INDICATOR OF TRANSMISSIBILITY)

    • -TRANSMITTED VIA BLOOD, SEX, AND
    • PREGNANCY

    • -ONE SEROTYPE (BASED ON HBSAG)
    • REGARDING VACCINES; 4 SEROTYPES EPIDEMIOLOGICALLY

    -CYTOTOXIC T CELLS

    • -HUMANS ARE ONLY RESERVOIR;
    • PARTICULARLY PROMINENT IN ASIA

    • -ABOUT 5% INFECTED BECOME CHRONIC
    • CARRIERS
  48. HEP C
    FLAVIVIRUS

    (+)ssRNA; ENV;

    6 SEROTYPES "C FOR CHYMERA"; HIGH MUTATION RATE

    LESS SEVERE THAN HEP B BUT MORE CHRONIC

    LIVER DAMAGE BY CYTOTOXIC T CELLS

    BLOOD; SEX

    • BLOCKS p53 "C FOR CANCER"
  49. HEP C TREATMENT
    • -DIAGNOSED BY DETECTING AB IN ELISA
    • (Ag IN ASSAY IS A RECOMBINANT PROTEIN FORMED FROM THREE IMMUNOLOGICALLY STABLE HCV PROTEINS AND DOES NOT INCLUDE HIGHLY VARIABLE ENVELOPE PROTEINS)

    • B/C FALSE + CAN OCCUR, RIBA SHOULD
    • BE PERFORMED AS A CONFIRMATORY TEST

    • -TREATMENT OF ACUTE HEP C WITH
    • ALPHA INTERFERON DECREASES THE # OF PTS THAT BECOME CHRONIC CARRIERS

    • -TREATMENT FOR CHRONIC CARRIERS IS
    • COMBINATION OF PEGINTERFEREON (PEGASYS) AND RIBAVIRIN
  50. HEP D
    DELTA VIRUS

    Enveloped, (-) ssRNA, covalently closed circle

    -SIMILAR TO HBV

    -HDV AND HBV WORSE BUT CHRONIC HEP IS ABOUT THE SAME

    - DEFECTIVE VIRUS (CANNOT REPLICATE BY ITSELF BECAUSE IT DOES NOT HAVE ANY GENES FOR ENVELOPE PROTEIN)

    -GENOME ENCODES ONLY ONE PROTEIN, INTERNAL CORE PROTEIN CALLED DELTA ANTIGEN

    -RNA IS RIBOZYME; HAS ABILITY TO SELF-CLEAVE AND SELF-LIGATE

    -REPLICATION IN NUCLEUS

    -ONE SEROTYPE (LIKE HBV)

    -HUMANS ONLY RESERVOIR

    -TRANSMITTED SAME AS HBV (BLOOD, SEX, PREGNANCY); PATHOGENESIS SAME AS HBV; DELTA ANTIGEN MAY BE CYTOPATHIC FOR HEPATOCYTES

    -IMMUNITY UNCERTAIN BECAUSE IgG AGAINST DELTA Ag NOT DETECTED FOR LONG PERIODS AFTER INFECTION
  51. HEP B TREATMENT
    VACCINE

    ADEFOVIR

    a-INF

    LAMIVUDINE
  52. ADENOVIRUS (PERSISTANT)
    LINEAR dsDNA

    FIBER AND PENTON BIND TO INTEGRINS

    41 SEROTYPES

    NUC ALONG MICROTUBULES

    CAUSE PERSISTANT INFECTION

    HOST RNA POL II --> E1A --> ACTIVATES EARLY & CELL GENES TO READY FOR REPLICATION --> E2 HAS VIRAL DNA POL FOR REP

    E1A DELAYED EARLY AND LATE GENES L1-L5 FOR STRUCT PROTS (ALSO p53 AND Rb) --> SELF ASSEMB IN NUC --> HOST PROT SYNTH SHUT OFF --> LYSIS

    E1B AND E3 BLOCK CTL MED APOP AND MHC I

    LATENT INFECT GI & LYMPH

    3,4,7,21 LRT PNEMONIA OR ACUTE RESP DISEASE (ARD) IN KIDS & OVERCROWDED FATIGUED POPS

    11,21 --> ACUTE HEM CYSTITIS, VIREMIA HEMATURIA NO FEVER MAINLY BOYS (KIDNEY)

    40,41 --> GI

    8,19 --> CONJUNCTIVITIS; EPIDEMIC KERATO-CONJUNCT

    SHELL VIAL ASSAY
  53. HPV
    cdsDNA; NON-ENV; HISTONES; CAP PROT L1

    >100 SEROTYPES

    16,18,31,45 --> CERVICAL CARCINOMA

    1. ATTACHES TO INTEGRINS, ENDOCYTOSIS

    2. UNCOATING BY ACIDIFICATION

    3. REPLICATION IN NUC VIA CELL’S DNA POLY AND RNA POL

    5. E4 DISRUPTS CYTOKERATINS TO ALLOW EXIT DURING KOILOCYTOSIS (LYSIS?)

    • 1. INFECTS EPIDERMAL CELLS AND
    • CAUSES KOILOCYTES

    GEN-URO CONDYLOMAS IMPEDE

    2. INFECT BASAL LAYER BUT NO VIRUS MADE; MADE IN SUPERFICIAL LAYER

    3. SKIN-TO-SKIN CONTACT OR GENITAL CONTACT

    4. NO VIREMIA

    3. E6 INACTIVATE P53 AND E7 INACTIVATES POCKET PROTEINS PRB, P107, AND P130 DRIVES CELLS TO S PHASE

    1. BOTH CMI AND Ab ARE INDUCED BY VIRAL INFECTION

    2. DNA HYBRIDIZATION TESTS TO DETECT PRESENCE OF VIRAL DNA

    1. DESTROY WARTS WITH CHEMICALS (PODOPHYLLIN), CRYOSURGERY, LASER, ELECTRO

    2. a-IFN (GOOD AT PREVENTING RECURRING INFECTIONS)

    3. IMMUNE RESPONSE MODULATORS (IMIQUIMOD)

    3. GARDASIL VACCINE (APPROVED FOR WOMEN 9-26)-CONTAINS L1 CAPSID PROTEINS FOR TYPES 6,11,16,18

    4. CERVARVIX-L1 AGAINST 16,18,31,45

    2. SKIN WARTS-TYPES 1-4

    3. GENITAL WARTS-TYPES 6 AND 11 (30 TYPES INFECT GENITAL TRACT)
  54. POLYOMAVIRUS
    cdsDNA; NON-ENV; HISTONES; ICOSA

    1. ADSORPTION TO GLYCOPROTEINS (ASTROCYTES/OLIGODENDROCYTES IN JC, KIDNEY IN BK)

    2. UNCOATING AS GENOME IS INJECTED INTO NUCLEUS

    3. REPLICATION IN NUC

    4. ASSEMBLY IN CYTO THEN NUC

    5. RELEASE BY VESICULAR EXOCYTOSIS

    1. INFECT MUCOSAL EPI AND SPREADS BY VIREMIA TO TARGET TISSUES

    2. TRANSMISSION-RESPIRATORY

    4. NATURAL HOST IS MOUSE

    2. INTEGRATES INTO CELL DNA AND ONLY EARLY PROTEINS ARE MADE, INCLUDING T Ag (REQUIRED FOR MAINTENANCE OF TRANSFORMED STATE)

    3. LYTIC/PERSISTENT

    4. OFTEN MILD OR ASYMPTOMATIC; POSSIBILITY OF LIFE-LONG INFECTIONS OF CARRIERS WHO SHED VIRUS IN URINE

    5. BK CAUSES KIDNEY CYSTITIS, NEPHRITIS, AND KIDNEY ALLOGRAFT FAILURE

    JC PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY-DUE TO OLIGODENDROCYTE AND ASTROCYTE DESTRUCTION (CAN INFECT B CELLS ALSO)

    INFLAMMATION CAN RESULT IN PLAQUES OF DEMYELINATION

    HEMIPARESIS, DEMENTIA, VISUAL SENSORY FXN LOSS; MOST PATIENTS DIE WITHIN 6 MONTHS (DISEASE OCCURS WHEN LATENT JC VIRUS IS ACTIVATED IN AN IMMUNO-COMPROMISED PATIENT)

    SV40 VIRUS CAUSES MALIGNANT TUMORS IN NON-HUMAN SPECIES SUCH AS HAMSTERS

    DEFENSES: SERUM Ab, CMI
  55. TREAT POLYOMAVIRUS
    DIAGNOSIS

    1. SX TRIAD

    2. CNS LESIONS ON CT/MRI

    3. IMMUNO-STAINING, PCR

    4. HA INHIBITION

    TREATMENT:

    1. PML TX WITH IFN-ALPHA, CIDOFOVIR, ARA-C, HAART, AZT

    1.NO VACCINE

    1. JCV NOT A PROBLEM FOR HEALTHY PPL

    • 2. INFECTIONS
    • ARE COMMON WORLDWIDE

    3. OCCUR IN EARLY CHILDHOOD

    VIRUS PERSISTS IN KIDNEY, TONSILS, LYMPHOCYTES
  56. HTLV VIRUS
    RETROVIRUS

    2. 2 ssRNA GENOMES

    3. ENV HELICAL; gp21 AND gp46 SURFACE PROTEINS

    VIRUS BINDS TO CD4 T CELLS OR DEND CELLS, FUSING WITH CELL MEMBRANE

    VIRION UNCOATING ACTIVATES REVERSE TRANSCRIPTASE (RT) TO MAKE CDNA

    cDNA TRAVELS TO NUC, WAITS FOR MITOSIS, INTEGRATES INTO HOST GENOME

    HOST RNA POL II

    TL IN CYTOPLASM

    ASSEMBLY IN CYTOPLASM; BUDDING

    1. INFECTS T CELLS OR DENDRITIC CELLS (LYMPHOID TISSUE), TRAVELS THROUGH BLOOD TO OTHER TISSUES

    SEXUAL CONTACT AND BLOOD

    TRANSFEROF ENTIRE INFECTED CELLS!!!!

    HAM/TSP

    INFECTS SPINAL CORD T-CELLS, CAUSE SPASTIC GAIT AND BLADDER DYSFUNC.

    EXCLUDE MS; TEST CSF

    HTLV INFECTS T CELLS BUT DOES NOT KILL THEM; IMMORTALIZES THEM BY MALIGNANT TRANSFORMATION

    ATL

    TAX ACTIVATES IL-2 AND IL-2 RECEPTOR WHICH CAUSES RAPID T-CELL GROWTH AND EVENTUAL MALIGNANT

    STIMULATES ONCOGENESIS

    USUALLY MONOCLONAL

    • SX OF LYMPHADENOPATHY, HEPATOSPLENOMEGALY, LYTIC BONE LESIONS, AND SKIN LESIONS
    • (PROLIFERATING T CELLS INFILTRATING THESE ORGANS-T CELLS HAVE DISTINCTIVE FLOWER-SHAPED NUCLEI)

    HYPERCALCEMIA DUE TO INCREASED OSTEOCLAST ACTIVITY

    REDUCED CMI, OPPORTUNISTIC INFECTIONS

    HTLV-ASSOCIATED PROGRESSIVE MYELOPATHY

    DEMYELINATING DISEASE OF BRAIN AND SPINAL CORD, MOTOR NEURONS IN SPINAL CORD; CD8 T CELLS DIRECTED AGAINST HTLV Ag ACCUMULATE IN CSF

    EITHER CAUSED BY AUTOIMMUNE CROSS-REACTION IN WHICH THE IMMUNE RESPONSE AGAINST HTLV DAMAGES NEURONS, OR BY CTL ATTACK OF HTLV-INFECTED NEURONS

    SX (AFTER AGE 30) OF GAIT DISTURBANCE, WEAKNESS OF LOWER LIMBS; LOSS OF BOWEL AND BLADDER CONTROL (BLADDER SX OF URINARY FREQUENCY, URGENCY, INCONTINENCE, ETC) *LOSS OF MOTOR FUNCTION MUCH GREATER THAN SENSORY LOSS

    • PARAPARESIS MAY INITIALLY BE ASYMMETRICAL BUT EVENTUALLY PROGRESSES TO SYMMETRICAL SPASTIC
    • GAIT

    BACK PAIN, CONSTIPATION, SEXUAL DYSFXN COMMON

    • PTS MAY ALSO HAVE UVEITIS, ARTHRITIS,
    • POLYMYOSITIS, KERATOCONJUNCTIVITIS SICCA (DRYNESS OF CORNEA AND CONJUNCTIVA), AND INFECTIOUS DERMATITIS


    • v.
    • PRINCIPLE HOST DEFENSE

    • 1.
    • Ab AGAINST HTLV

    CD8 T CELLS
  57. TREAT HTLV
    DIAGNOSIS: Ab AGAINST VIRUS IN ELISA (WESTERN BLOT TO CONFIRM)

    PCR FOR HTLV RNA OR DNA WITHIN INFECTED CELLS

    ATL DIAGNOSED BY FINDING MALIGNANT T CELLS IN LESIONS

    HAM DIAGNOSED BY PRESENCE OF Ab IN CSF

    NO ANTIVIRAL THERAPY

    ATL TREATED WITH ANTICANCER CHEMO

    HAM-CORTICOSTEROID AND DANAZOL PROVIDES SOME HELP

    NO VACCINE

    SCREENING DONATED BLOOD

    CONDOMS

    NO BREAST FEEDING FOR WOMEN WITH HTLV AB’S

    INTERESTING FACTS ABOUT VIRUS

    • STRUCTURE: *GAG (STRUCTURAL PROTEINS), *POL (REVERSE TRANSCRIPTASE, INTEGRASE, PROTEASE), *ENV (ENVELOPE PROTEINS), PLUS TWO REGULATORY GENES TAX (TC
    • ACTIVATOR SIMILAR TO TAT OF HIV) AND REX (GOVERNS PROCESSING OF VIRAL MRNA AND ITS EXPORT FROM NUCLEUS TO CYTOPLASM)

    • DIFFERENCES BETWEEN HIV AND HTLV-DIFFERENT REGULATORY GENES, DIFFERENT p24 NUCLEOCAPSID PROTEIN (IMPORTANT PROTEIN BECAUSE
    • THIS IS THE ONE THAT MANY AB’S ARE MADE AGAINST), AND DIFFERENT SURFACE
    • PROTEINS (GP21/46 FOR HTLV, GP120/41 FOR HIV)
  58. HIV
    • 1. RETROVIRUS-LENTIVIRUS
    • GROUP (SLOW INFECTIONS WITH LONG INCUBATION PERIODS)

    2. 2 ssRNA; ENV HELICAL CAPSID WITH GP120 AND GP41 SURFACE PROTEINS

    1. GP120 ATTACHES TO CD4 RECEPTOR ON T CELLS (CCR5 ON MACROPHAGES AND CXCR4 ON T CELLS ACT AS CO-RECEPTORS)

    2. GP41 MEDIATES FUSION OF THE VIRAL ENVELOPE WITH THE PM

    3. VIRAL GENOME DELIVERED INTO CYTOPLASM UPON UNCOATING

    4. RNA TO CDNA BY RT IN CYTO

    5. cDNA TRANSPORTED TO NUC (VIA Vpr) AND INTEGRATED INTO HOST GENOME (VIA INTEGRASE)

    6. CELLULAR RNA POL II INTERACTS WITH LTR (Tat) TO TC GENOME INTO VIRAL MRNA

    7. mRNA TRANSPORTED TO CYTO TO BE TL INTO PROTS (VIA Rev)

    8. PROTS CLEAVED INTO FINAL FRAGMENTS BY VIRAL PROTEASE

    9. ASSEMBLY ON PM (NEED Vpu)

    10. BUDDING

    ROUTE OF INFECTION

    1. TRAUMATIZED MUCOUS MEMBRANE THAT ALLOWS GP120 OF HIV TO INTERACT WITH DC-SIGN OF DEND CELLS


    • 2. DEND CELLS TRAVEL TO LNs à
    • CD4 T CELLS

    3. INFECTED BLOOD, SEXUAL CONTACT, PERINATAL

    SYMPTOMS AND HALLMARKS OF DISEASE

    1. PROVIRUSES MIGRATE TO LYMPHOID TISSUES WHERE THEY CAN REMAIN LATENT

    2. VIRUS ABLE TO EVADE HOST DEFENSE

    a. INTEGRATION INTO HOST GENOME

    b. Tat AND Nef PROTS DOWN-REGULATE MHC CLASS I EXPRESSION

    c. HIGH MUTATION OF ENV GENE (Ag VARIATION)

    3. INITIAL VIREMIA HIGH-SETS VIRAL LOAD (DETERMINES LIKELIHOOD OF PROGRESSION TO FULL-BLOWN AIDS)

    4. ALSO TARGETS CD4 TH17 CELLS-LEADING TO LOSS OF MUCOSAL IMMUNITY AND INCREASED SUSCEPTIBILITY TO BLOOD STREAM INFECTIONS BY BACTERIA IN NORMAL FLORA (E COLI)

    • 5. VIRUS ALSO TARGETS BRAIN MONOCYTES AND MACROPHAGES-FORM OF MULTI-NUCLEATED GIANT
    • CELLS THAT CAUSE CNS SX

    6. HIV INFECTION DIVIDED INTO 3 STAGES:

    a. ACUTE STAGE-BEGINS 2-4 WKS AFTER INFECTION; A MONO-TYPE PICTURE OF FEVER, LETHARGY, SORE THROAT, AND GENERALIZED LYMPHADENOPATHY (MAY SEE MACULOPAPULAR RASH ON TRUNK, ARMS, LEGS)

    LEUKOPENIA OCCURS

    HIGH VIREMIA

    INFECTION IS READILY TRANSMISSIBLE

    RESOLVES SPONTANEOUSLY IN ABOUT 2 WKS BY ACTION OF CD8 T CELLS

    Ab APPEARS ABOUT 10-14 DAYS AFTER INFECTION

    b. MIDDLE STAGE

    LONG LATENT INFECTION, LASTING FOR YEARS

    PT IS ASYMPTOMATIC AND VIREMIA LOW; HOWEVER, VIRUS ITSELF IS NOT LATENT, BECAUSE VIRUS IS MAKING MORE OF ITSELF AND STAYING SEQUESTERED IN LN’S

    CAN SEE AIDS-RELATED COMPLEX-PERSISENT FEVERS, FATIGUE, WEIGHT LOSS, AND LYMPHADENOPATHY (USUALLY PROGRESSES TO AIDS)

    c. LATE STAGE-AIDS

    CD4 T CELL COUNT BELOW 400 (CAN USE THIS TO TRACK INFECTION)

    INCREASE IN FREQUENCY AND SEVERITY OF OPPORTUNISTIC INFECTION, MOST COMMON OF WHICH ARE PNEUMOCYSTIS PNEUMONIA AND KAPOSI’S SARCOMA

    PRINCIPLE HOST DEFENSE

    1. INNATE IMMUNITY

    2. CD8 T CELL ATTACK

    ALPHA-DEFENSINS (BLOCK BINDING TO CXCR4 RECEPTOR)
  59. TREAT HIV
    DIAGNOSIS

    1. DETECTION OF AB IN ELISA (GIVES MANY FALSE-POSITIVES SO DO A WESTERN BLOT TO CONFIRM; AB AGAINST P24, GP41)

    2. ORAQUICK-BLOOD SAMPLE OBTAINED BY FINGERPRICK; RAPID IMMUNOASSAY FOR HIV AB AVAILABLE IN 20 MIN

    3. PCR TO DETECT HIV DNA

    TREATMENT

    • 1. HAART-EITHER 2 NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS (LIKE LAMIVUDINE, ZIDOVUDINE) AND
    • ONE PROTEASE INHIBITOR (FOSAMPRENAVIR) OR 2 NRTI’S AND ONE NON-NUCLEOSIDE RT INHIBITOR (EFAVIRENZ)

    PREVENTION

    1. NO VACCINE

    2. CONDOMS, SCREEN DONATED BLOOD, NO SHARING NEEDLES

    3. ZDV OR NEVIRAPINE GIVEN PERINATALLY TO INFECTED MOMS AND NEONATES; NO BREAST FEEDING; C-SECTION

    INTERESTING FACTS ABOUT VIRUS

    1. STRUCTURE OF GENOME-GAG, POL, ENV, VPR, VPU, REV, TAT, VIF (INHIBITING ACTION OF ENZYME THAT CAUSES HYPERMUTATION IN RETROVIRAL DNA AND INACTIVATES IT) , NEF

    • 2. TYPES-HIV 1 (FROM CHIMP) CAUSES MOST AIDS CASES AND IS FURTHER CLASSIFIED INTO SUBTYPES/CLADES (GOOD FOR STUDYING REGIONAL PATTERNS), HIV 2 (FROM SOOTY
    • MANGABEY)

    KAPOSI’S SARCOMA

    1. CAUSED BY HERPES VIRUS

    2. ONE OF THE MOST COMMON OPPORTUNISTIC INFECTIONS SEEN IN AIDS PATIENTS

    3. PRIMARY INFECTION LIKELY TO BE FEBRILE ILLNESS

    • 4. MAINLY INFECTS B CELLS AND VASCULAR ENDOTHELIAL CELLS (AB AND CMI DEVELOP AND RESTRICT
    • LATENT AND LYTIC INFECTIONS BUT CAN’T CLEAR VIRUS)

    5. 3 TYPES:

    a. CLASSIC KS (ELDERLY MEDITERRANEAN MALES)

    b. ENDEMIC KS (CENTRAL AFRICAN CHILDREN)

    c. AIDS-ASSOCIATED KS

    • ENDOTHELIAL CELL TUMOR-CELLS ARE TRANSFORMED DUE TO INACTIVATION OF P53 AND POCKET PROTEINS; ALSO PRODUCTION OF KAPOSINS THAT ACTIVATE SIGNALING PATHWAYS TO
    • STIMULATE CELL GROWTH

    ALSO MAY ENCODE ANTI-APOPTOTIC PROTEINS THAT RESIST CTL KILLING

    CAUSE CHARACTERISTIC PURPLE SKIN LESIONS

    DIAGNOSIS BY OBSERVATION, BIOPSY; ELISA, WESTERN BLOT, IMMUNOFLUORESCENCE TO DETECT AB TO KSHV PROTEINS

    TX WITH HAART, REMOVE LESIONS BY SURGERY, RADIATION, IFN, OR VINBLASTINE
  60. HSV-1
    1. HERPES VIRUS -ALPHA GROUP

    2. LINEAR dsDNA GENOME

    • 3. ENVELOPED
    • ICOSAHEDRAL CAPSID

    LIFE CYCLE

    1. BINDS TO HEPARAN SULFATE ON CELL MEMBRANE AS RECEPTOR AND BINDS TO 2ND RECEPTOR, NECTIN

    • 2. VIRION ENVELOPE FUSES WITH PLASMA MEMBRANE AND RELEASES GENOME + TEGUMENT PROTEIN INTO
    • CYTO

    3. GENOME DNA AND TEGUMENT PROTEIN (VP16) GET INTO NUCLEUS BY DOCKING TO NUCLEAR PORE

    4. LINEAR dsDNA BECOMES CIRCULAR; VP16 INTERACTS WITH TC FACTORS TO INITIATE TC OF IE GENES OF DNA

    5. TL OF IE PROTEINS (NON-STRUCTURAL PROTEINS) IN CYTO

    6. ACTIVATION OF TC AND TL OF E PROTEINS (DNA POL AND THYMIDINE KINASE)

    7. VIRAL DNA POL REPLICATES GENOME DNA

    8. TC AND TL OF L PROTEINS (STRUCTURAL PROTEINS)-TO NUCLEUS

    9. ASSEMBLY IN NUCLEUS

    10. BUDDING FROM NUCLEAR MEMBRANE AND EXIT BY TUBULES AND VACUOLES

    ROUTE OF INFECTION

    1. HSV REPLICATES IN EPITHELIAL CELLS, ACCESSES NERVE ENDINGS, AND IS TRANSPORTED RETROGRADE TO NEURON NUCLEI

    2. HSV-1=TRANSMITTED BY SALIVA

    MOST COMMON USA CAUSE OF ENCEPHALITIS

    3. HSV-2=TRANSMITTED BY SEXUAL CONTACT

    4. BOTH HAVE ASYMPTOMATIC SHEDDING

    SYMPTOMS AND HALLMARKS OF DISEASE

    1. PRIMARY INFECTION PUTS VIRUS IN SENSORY GANGLIA (TRIGEMINAL IN HSV-1 AND LUMBAR AND SACRAL GANGLIA IN HSV-2); INFECTION ACTIVATES A POTENT IMMUNE RESPONSE THAT RESTRICTS SPREAD AND RESOLVES SX (VIRUS NOT GONE)

    2. LATENT INFECTION:

    a. HSV PERSISTS AS CIRCULAR DNA IN NUCLEUS (NOT INTEGRATED INTO GENOME)

    b. TC LAT’S (LATENCY ASSOCIATED TRANSCRIPTS) THAT BLOCK VIRAL REPLICATION

    c. IMMUNE EVASION BY NEURONS THAT ARE BEHIND THE BLOOD-BRAIN BARRIER, EXPRESS LOW LEVELS OF MHC AND DIVIDE INFREQUENTLY

    • 3. REACTIVATION: LYTIC INFECTION INDUCED BY UV EXPOSURE, STRESS, HORMONE CHANGES, ETC. (ENABLES
    • SHEDDING FROM EPI CELLS)

    4. HSV-1

    a. 2-12 DAY INCUBATION PERIOD THEN PRESENT WITH FEVER, PHARYNGITIS, MALAISE, EDEMA, ETC. (SKIN LESIONS USUALLY RESOLVE)

    • b. GINGIVOSTOMATOSIS-PRIMARILY
    • IN KIDS; FEVER, IRRITABILITY, VESICULAR LESIONS IN MOUTH (RESOLVE IN 2-3 WKS)

    • c. HERPES LABIALIS (COLD SORE)-MILDER, RECURRENT FORM WITH CROPS OF LESIONS AT MUCOCUTANEOUS
    • JXN OF LIPS OR NOSE

    • d. KERATOCONJUNCTIVITIS-CORNEAL
    • ULCERS AND LESIONS OF CONJUNCTIVIAL EPI (RECURRENCES-SCARRING, BLINDNESS)

    e. ENCEPHALITIS

    NECROTIC LESION IN ONE TEMPORAL LOBE

    FEVER, HEADACHE, VOMITING, SEIZURES, ALTERED MENTAL STATUS (ACUTE OR PROTRACTED OVER SEVERAL DAYS)

    EXAMINATION OF CSF SHOWS MODERATE INCREASE IN LYMPHOCYTES, ELEVATION IN PROTEINS, AND NORMAL GLUCOSE

    HIGH MORTALITY RATE AND SEVERE NEUROLOGICAL SEQUELAE IN THOSE WHO SURVIVE

    HERPETIC WHITLOW-PUSTULAR LESION OF SKIN OF FINGER OR HAND (MEDICAL PERSONNEL IN CONTACT WITH PATIENT’S LESIONS)

    g. HERPES GLADIATORUM-OCCURS IN WRESTLERS OR PPL WITH CLOSE BODY CONTACT; VESICULAR LESIONS ON HEAD, NECK, AND TRUNK

    DISSEMINATED INFECTIONS IN IMMUNOCOMPROMISED PATIENTS WITH DEPRESSED T-CELL FXN
  61. HSV-2
    LARGE

    dsDNA, ENV

    TEGUMENT

    a. GENITAL HERPES-PAINFUL VESICULAR LESIONS OF MALE AND FEMALE GENITALIA AND ANAL AREA (PRIMARY INFECTION ASSOC. WITH FEVER AND INGUINAL ADENOPATHY)

    • b. NEONATAL HERPES-CONTACT WITH VESICULAR LESIONS OF BIRTH CANAL-RANGE FROM SEVERE
    • ENCEPHALITIS OR DISSEMINATED LESIONS TO MILDER LOCAL LESIONS OF SKIN,ETC. TO ASYMPTOMATIC INFECTION

    c. ASEPTIC MENINGITIS-MILD, SELF-LIMITING

    2. BOTH TYPES 1 AND 2 ARE ASSOCIATED WITH ERYTHEMA MUTLIFORME-“TARGET” LESION ON TRUNK, HANDS, AND FEET (THOUGHT TO BE IMMUNE-MEDIATE RXN TO HSV AG)
  62. TREAT HSV 1&2
    PRINCIPLE HOST DEFENSE

    1. IMMUNITY IS TYPE-SPECIFIC, BUT SOME CROSS-RXN CAN OCCUR

    2. IMMUNITY IS INCOMPLETE, IGG

    3. CMI MORE IMPORTANT

    DIAGNOSIS

    1. ISOLATION OF VIRUS FROM LESION BY GROWTH IN CELL CULTURE (VERIFY BY ELISA)

    • 2. TZANCK SMEAR-RAPID DX, LOOK FOR
    • MULTINUCLEATED GIANT CELLS

    3. PCR


    4. SEROLOGICAL TESTING FOR PRIMARY INFECTION

    TREATMENT

    1. ACYCLOVIR-SHORTENS DURATION OF LESION AND REDUCES EXTENT OF SHEDDING

    2. FOSCARNET IF RESISTANT TO ACYCLOVIR

    3. VALTREX, FAMVIR

    4. CAN’T CURE LATENT STATE

    PREVENTION

    1. AVOIDING CONTACT WITH VESICULAR LESION OR ULCER

    2. C-SECTION FOR MOMS AT TERM WITH GENITAL LESIONS OR POSITIVE VIRAL CULTURES

    INTERESTING FACTS ABOUT VIRUS

    1. HSV MOST COMMON CAUSE OF SPORADIC ENCEPHALITIS

    2. PRIMARY INFECTIONS ALWAYS WORSE THAN RECURRENT INFXN
  63. HERP SUB-FAMILIES
    ALPHA - WIDE HOST RANGE, RAPID REPLICATION, NERVOUS SYSTEM. ex HSV-1&2, VARICELLA ZOSTER, CELL DISTRUCTION CPE!

    BETA - NARROW HOST RANGE, SLOW REP, IMMUNE SYSTEM. ex CMV, ROSEOLOVIRUS (HHV 6-7)

    GAMMA - NARROW HOST RANGE, MOD RAPID REP, IMMUNE SYSTEM AND TUMOR DEV. ex EBV, KSHV
  64. HERP CPEs
    LYTIC

    SHUT OFF HOST PROT SYNTH

    OWL-EYE

    FUSION (SYNCYTIA)
  65. EBV
    1. HERPES VIRUS FAMILY-GAMMA GROUP

    2. LINEAR dsDNA

    3. ENVELOPED ICOSAHEDRAL CAPSID

    TEGUMENT

    MOST COMMON INFECTION WORLDWIDE; 90% ADULTS USA

    OWL'S-EYE

    LIFE CYCLE SEE HSV

    • 1. TRANSMITTED IN SALIVA, LYTIC VIRUS INFECTION OF MUCOSAL EPITHELIUM ENABLES SPREAD IN BLOOD
    • OR LYMPH (TO GET TO B CELLS)

    2. ESTABLISHES LATENT INFECTION IN B CELLS-DNA IN NUCLEUS AND IS NOT INTEGRATED INTO GENOME

    SYMPTOMS AND HALLMARKS OF DISEASE

    • 1. CIRCULAR DNA IN THE NUCLEUS EXPRESSES GENE PRODUCTS THAT MAINTAIN/REPLICATE EBV DNA OR
    • TRANSFORM THE B CELLS INTO AN INDEFINITELY PROLIFERATING CELLS LINE

    2. INFECTIOUS MONONUCLEOSIS

    a. PRIMARY DISEASE OF YOUNG ADULTS/ADOLESCENTS ATTRIBUTED TO HIGHER LEVELS OF VIRUS TRANSMISSION DURING INTIMATE ORAL CONTACT

    b. SX OF FEVER, LYMPHADENOPATHY, MALAISE, HEADACHE, HETEROPHILE AB, T CELL LYMPHOCYTOSIS, NUCLEAR ATYPICAL T CELLS, RASH (EXACERBATED BY PENICILLIN), ENLARGED LIVER OR SPLEEN, WEIGHT LOSS

    c. RECOVER IN WEEKS TO MONTHS IS TYPICAL

    3. ORAL HAIRY LEUKOPLAKIA-IN AIDS PATIENTS; LYTIC EBV-INFECTED CELLS ALONG TONGUE (LIKE CANDIDA BUT NOT EASY TO SCRAPE OFF)

    4. LYMPHOPROLIFERATIVEDISEASE-NON-HODGKIN’S LYMPHOMA IN IMMUNE SUPPRESSED TRANSPLANT RECIPIENTS AND AIDS PTS. (MALIGNANT CELLS ARE LATENT EBV TRANSFORMED B-CELLS)

    PRINCIPLE HOST DEFENSE

    1. FIRST IGM AB TO VCA (VIRAL CAPSID ANTIGEN)

    2. IgG AB FOLLOWS AND PERSISTS FOR LIFE

    3. HETEROPHIL

    DIAGNOSIS

    1. CLINICAL SYMPTOMS

    2. SMEAR-ATYPICAL LYMPHS

    3. MONOSPOT ELISA-DETECT HETEROPHIL AB

    4. ELISA FOR EBV-SPECIFIC IGM OR IGG
  66. TREAT EBV
    NO ANTIVIRAL THERAPY

    2. HIGH-DOSE ACYCLOVIR FOR LIFE-THREATENING INFECTIONS

    PREVENTION

    1. NO VACCINE

    INTERESTING FACTS ABOUT VIRUS

    1. CANCERS OF LYMPHOID ORIGIN ASSOCIATED WITH EBV: NASOPHARYNGEAL CARCINOMA (SOUTH CHINA AND SOUTHEAST ASIA), BURKITT’S LYMPHOMA (CHROMOSOME TRANSLOCATION OF IG GENE ENHANCER DRIVING EXPRESSION OF C-MYC PROTO-ONCOGENE); HODGKIN’S LYMPHOMA (MALIGNANT B CELLS; DEFECTIVE INHIBITOR OF NF-KB THAT REGULATES TC)
  67. CYTOMEGALOVIRUS (CMV)
    1. HERPES VIRUS FAMILY-BETA GROUP

    2. LINEAR dsDNA, ENV, ICOSA

    ROUTE OF INFECTION

    1. EARLY IN LIFE-TRANSMITTED ACROSS PLACENTA, WITHIN BIRTH CANAL, AND BREAST MILK

    2. CHILDHOOD=SALIVA

    3. ADULTS-SEXUAL TRANSMISSION (SEMINAL AND CERVICAL SECRETIONS), BLOOD TRANSFUSIONS, TRANSPLANTS

    SYMPTOMS AND HALLMARKS OF DISEASE

    1. INFECTION IN CHILDREN AND ADULTS USUALLY ASYMPTOMATIC, EXCEPT IN IMMUNOCOMPROMISED INDIVIDUALS (LATENT STATE IN LEUKOCYTES THAT CAN BE RE-ACTIVATED WHEN CMI IS LOW)

    2. INFECTION IN FETUS CAUSE CYTOMEGALIC INCLUSION DISEASE

    a. CHARACTERIZED BY MULTINUCLEATED GIANT CELLS WITH PROMINENT INTRANUCLEAR INCLUSIONS (OWL’S EYE INCLUSIONS)

    b. AFFECTS MANY ORGANS AND WIDESPREAD CONGENITAL ABNORMALITIES RESULT-DURING MOM’S PRIMARY INFECTION AND WORSE IF DURING 1ST TRIMESTER

    c. SX OF MICROCEPHALY, SEIZURES, DEAFNESS, JAUNDICE, AND PURPURA, HEPATOSPLENOMEGALY, MR

    3. HETEROPHIL-NEGATIVE MONONUCLEOSIS IN IMMUNOCOMPETENT ADULTS-FEVER, LETHARGY, PRESENCE OF ABNORMAL LYMPHOCYTES IN BLOOD SMEAR

    4. SYSTEMIC CMV INFECTIONS, ESPECIALLY PNEUMONITIS, HEPATITIS, RETINITIS IN IMMUNOSUPPRESSED PATIENTS (AIDS, TRANSPLANT RECIPIENTS)

    PRINCIPLE HOST DEFENSE

    1. CIRCULATING AB AND CMI

    DIAGNOSIS

    1. SHELL VIAL ASSAY (CULTURE VIRUS) COUPLED WITH USE OF IMMUNOFLUORESCENT AB

    2. FLUORESCENT AB AND HISTOLOGICAL STAINING OF INCLUSION BODIES-OWL’S EYE SHAPE

    3. PP65 AG DETECTION WITHIN BLOOD LEUKOCYTES USING IMMUNOFLUORESCENCE ASSAY
  68. TREAT CMV
    1. GANCICLOVIR, VALGANCICLOVIR, FOSCARNET, CIDOFOVIR, FOMIVIRSEN

    PREVENTION

    1. NO VACCINE

    2. ISOLATION OF INFECTED INFANTS

    3. ONLY CMV-NEGATIVE TRANSPLANT DONORS AND BLOOD DONORS

    • HIGH TITER IMMUNE GLOBULIN (CYTOGAM) TO PREVENT DISSEMINATED
    • CMV INFECTION IN TRANSPLANT RECIPIENTS
  69. VARICELLA-ZOSTER
    1. HERPES VIRUS-ALPHA GROUP

    2. LINEAR dsDNA, ENV, ICOSA

    ROUTE OF INFECTION

    1. TRANSMITTED BY RESPIRATORY DROPLETS AND BY DIRECT CONTACT WITH LESIONS

    2. VARICELLA-PRIMARY DISEASE; ZOSTER/SHINGLES IS RECURRENT FORM

    SYMPTOMS AND HALLMARKS OF DISEASE

    1. VZV INFECTS MUCOSA OF URT THEN SPREADS VIA BLOOD TO SKIN, WHERE TYPICAL VESICULAR RASH OCCURS

    2. MULTI-NUCLEATED GIANT CELLS WITH INTRANUCLEAR INCLUSIONS ARE AT BASE OF LESIONS

    3. VIRUS INFECTS SENSORY NEURONS AND IS CARRIED BY RETROGRADE FLOW TO DORSAL ROOT GANGLIA WHERE VIRUS BECOMES LATENT

    • 4. LATENTLY INFECTED CELLS-DNA IN NUCLEUS AND NOT INTEGRATED INTO GENOME; LATER IN TIMES OF REDUCED CMI OR TRAUMA, VIRUS IS REACTIVATED TO VESICULAR RASH AND NERVE PAIN OF
    • ZOSTER

    5. VARICELLA

    a. INCUBATION PERIOD 2-12 DAYS

    b. BRIEF PRODROMAL SX OF FEVER AND MALAISE

    c. PAPULOVESICULAR RASH APPEARS ON TRUNK AND SPREADS TO HEAD AND EXTREMITIES; ITCHING

    d. MILD IN CHILDREN AND SEVERE IN ADULTS

    e. POSSIBILITY OF REYE’S SYNDROME WITH ASPIRIN

    6. ZOSTER

    a. OCCURRENCE OF PAINFUL VESICLES ALONG THE COURSE OF A SENSORY NERVE OF HEAD OR TRUNK

    b. PAIN CAN LAST FOR WEEKS AND POSTZOSTER NEURALGIA CAN BE DEBILITATING

    c. LIFE-THREATENING DISSEMINATED INFECTIONS LIKE PNEUMONIA CAN OCCUR IN IMMUNOCOMPROMISED PATIENTS

    PRINCIPLE HOST DEFENSE

    1. IMMUNITY FOLLOWING VARICELLA IS LIFE-LONG: GETS VARICELLA ONLY ONCE AND ZOSTER USUALLY ONLY ONCE

    2. FREQUENCY OF ZOSTER INCREASES WITH AGE (WANING IMMUNITY)

    DIAGNOSIS

    1. CLINICAL OBSERVATIONS

    2. TZANCK SMEAR-LOOK FOR MULTINUCLEATED GIANT CELLS

    3. ISOLATION OF VIRUS IN CELL CULTURE AND IDENTIFICATION WITH SPECIFIC ANTISERUM
  70. TREAT VARICELLA-ZOSTER
    1. NO ANTIVIRAL THERAPY

    2. ACYCLOVIR-REDUCE DURATION AND SEVERITY

    3. FOSCARNET IF RESISTANT TO ACYCLOVIR

    4. FAMVIR, VALTREX-ACCELERATE HEALING OF ZOSTER LESIONS

    PREVENTION

    1. TWO VACCINES

    a. LIVE ATTENUATED VARIVAX-PREVENT VARICELLA

    b. LIVE ATTENUATED ZOSTAVAX-PREVENT ZOSTER (DOES NOT ERADICATE LATENT STATE)
  71. HHV 6 & 7
    1. HERPES VIRUS

    2. LINEAR dsDNA, ENV, ICOSA

    EXANTHEM SUBTUM OR ROSEOLA INFANTUM

    LIFE CYCLE SEE HSV

    HALLMARKS OF DISEASE

    1. PRIMARY INFECTION OCCURS EARLY IN LIFE AS MATERNAL AB TITERS DECLINE

    2. TRANSMITTED IN SALIVA; ENTERS THROUGH NASO- OR OROPHARYNGEAL MUCOSA

    3. MOTHER TO OFFSPRING TRANSMISSION CAN OCCUR BY INTRAUTERINE TRANSPLACENTAL ROUTE OR INTRAPARTUM CONTACT WITH VIRUS IN GENITAL TRACT SECRETIONS OR INFECTED MUCOSA

    4. REPLICATE SLOWLY AND INFECT MANY CELLS: MUCOSAL EPI CELLS (ENTRY AND SHEDDING), SALIVARY GLAND CELLS (SHEDDING), ENDOTHELIAL CELLS (RASH), AND MONONUCLEAR CELLS (6 LATENTLY INFECTS MACROPHAGES, 7 LATENTLY INFECTS CD4 CELLS)

    5. VIRUS SPREADS FROM MUCOSAL EPI TO BLOOD OR LYMPH TO LYMPHOID TISSUES AND ENDOTHELIAL CELLS (MULTIPLE SITES OF LATENCY)

    6. PRIMARY DISEASE: 1 WK INCUBATION THEN SUDDEN FEVER FOR SEVERAL DAYS, THEN SUDDEN RASH APPEARS ON TRUNK AS FEVER DECLINES

    8. TX OF ORDINARY SUPPORTIVE CARE

    9. SEROPREVALENCE INCREASES AFTER 6 MOS. OF AGE (MOST ARE SEROPOSITIVE BY 4 YEARS)

    10. NO VACCINE DUE TO DISEASE MILDNESS AND FEW COMPLICATIONS
  72. RABIES
    1. RHABDOVIRUS FAMILY

    2. (-) SSRNA

    • 3. ENVELOPED, BULLET-SHAPED VIRION, HELICAL CAPSID
    • RHABDOVIRUS

    BULLET; LARGE

    (-)ssRNA, ENV, HELICAL

    1. RABIES VIRUS ATTACHES TO ACETYLCHOLINE RECEPTOR ON CELL SURFACE

    2. ENTERS AT PM BY RECEPTOR-MEDIATED ENDOCYTOSIS

    3. AFTER UNCOATING FROM ENDOSOME, VIRAL RNA POL. SYNTHESIZES FIVE MRNA’S THAT CODE FOR VIRAL PROTEINS

    4. REPLICATION OF VIRAL GENOME BY VIRAL RNA POL.

    5. PROGENY RNA ASSEMBLED WITH VIRION PROTEINS IN CYTO

    6. ENVELOPE IS ACQUIRED BY BUDDING FROM PM

    ROUTE OF INFECTION

    • 1. TRANSMITTED BY BITE OF RABID ANIMAL THAT MANIFESTS AGGRESSIVE BEHAVIOR INDUCED BY ENCEPHALITIS (WILD ANIMALS-RACCOONS, SKUNKS, BATS, FOXES, COYOTES)-VIRUS IN
    • SALIVA

    2. NOT MANY CATS AND DOGS BECAUSE THEY HAVE BEEN IMMUNIZED

    3. SOME NON-BITE EXPOSURE BY AEROSOLS OF BAT SECRETIONS CONTAINING RABIES VIRUS

    4. NO VIREMIC STAGE

    SYMPTOMS AND HALLMARKS OF DISEASE

    1. LOCAL REPLICATION OF VIRUS AT SITE OF BITE (MUSCLE, CT)

    2. ATTACHMENT TO SENSORY NERVE ENDINGS BY ACH RECEPTOR AND TRANSPORT VIA AXONS TO CNS

    3. REPLICATION IN SPINAL CORD AND BRAIN (HIPPOCAMPUS) AND FORMATION OF NEGRI BODIES (EOSINOPHILIC INCLUSION BODIES IN INFECTED NEURONS)

    4. TRANSPORT THROUGH PERIPHERAL NERVES TO SALIVARY GLANDS (INCREASED SECRETION FOR TRANSMISSION) AND OTHER ORGANS (KIDNEY, LUNG, PANCREAS, EYE, SKIN, ETC)

    5. ENCEPHALITIS DEVELOPS WHILE IN CNS, NEURON DESTRUCTION AND DEMYELINATION

    • 6. VARIABLE INCUBATION PERIOD>PRODROMAL PERIOD OF FEVER, ANOREXIA, ETC.>CONFUSION,
    • LETHARGY, INCREASED SALIVATION, PAINFUL MUSCLE SPASMS UPON SWALLOWING (DEVELOP HYDROPHOBIA, DON’T WANT TO SWALLOW WATER BECAUSE IT IS TOO PAINFUL)>SEIZURES, PARALYSIS, COMA

    PRINCIPLE HOST DEFENSE

    1. NO REAL INFO BECAUSE MOST HAVE NOT SURVIVED TO ENDURE 2ND BITE

    DIAGNOSIS

    1. FLUORESCENT AB STAINING OF BIOPSY SPECIMEN, USUALLY TAKEN FROM SKIN OF NECK AT HAIRLINE

    2. ISOLATION OF VIRUS FROM SOURCES SUCH AS SALIVA

    3. RISE IN TITER OF AB TO VIRUS

    4. NEGRI BODIES DEMONSTRATED IN CORNEAL SCRAPINGS OR IN AUTOPSY SPECIMENS

    INTERESTING FACTS ABOUT VIRUS

    1. NEGRI BODIES

    2. WHILE IN NEURONS, VIRUS IS SHIELDED FROM IMMUNE SYSTEM (LACK OF IMMUNE RESPONSE)

    3. FURIOUS RABIES (80%) HYPERACTIVITY, AGGRESSIVENESS; VIRUS REPLICATES IN LIMBIC SYSTEM (INCLUDING HIPPOCAMPUS AND AMYGDALA) THAT CONTROLS EMOTION

    4. DUMB RABIES (20%)-PROGRESSIVE PARALYSIS; VIRUS REPLICATES IN NEOCORTEX (PART OF CEREBRAL CORTEX THAT GOVERNS CONSCIOUS THOUGHT AND LANGUAGE, ETC.)
  73. TREAT RABIES
    1. NO ANTIVIRAL THERAPY; JUST SUPPORTIVE CARE

    PREVENTION

    1. PRE-EXPOSURE=VACCINE GIVEN TO HIGH-RISK INDIVIDUALS (VETS)-3 DOSES

    2. POST-EXPOSURE=HUMAN DIPLOID CELL VACCINE (HDCV-INACTIVATED VIRUS) (5 DOSES) + HUMAN RABIES IMMUNE GLOBULIN (1 DOSE) GIVEN AT BITE SITE
  74. 3 CLINICAL SYMPTOMS FOR ARBOVIRUSES
    encephalitis,

    • hemorrhagic fever, mild fever with muscle and
    • joint pain

    non-hemorrhagic rash
  75. HANTAVIRUS
    BUNYA

    (-)ssRNA; ENV; 3 SEGS, HELICAL

    a. ROBOVIRUS-RODENT-BORNE

    • b. KOREAN HEMORRHAGIC FEVER (HEADACHE, PETECHIAL HEMORRHAGES,
    • SHOCK, RENAL FAILURE)

    c. RECENT OUTBREAK IN WESTERN US CHARACTERIZED BY FLU-LIKE SX FOLLOWED BY ACUTE RESPIRATORY FAILURE

    SIN NOMBRE VIRUS (IN DEER MICE)

    ACQUIRED BY INHALING AEROSOLS OF MICE URINE/FECES

    DIAGNOSIS BY DETECTING VIRAL RNA IN LUNG TISSUE WITH PCR ASSAY OR BY DETECTING IGM IN SERUM

    NO EFFECTIVE DRUG

    NO VACCINE
  76. WEST NILE
    FLAVIVIRUS

    (+) ssRNA NON-SEG; ENV, ICOSA

    a. WILD BIRDS (CROWS) ARE MAIN RESERVOIR AND VIRUS IS TRANSMITTED BY BITES OF CULEX MOSQUITOES

    b. FEVER, CONFUSION, STRIKING MUSCLE WEAKNESS (ENCEPHALITIS)

    c. LIFE CYCLE

    BINDING TO CELL RECEPTOR AND ENDOCYTOSIS

    VIRION-ENDOSOME MEMBRANE FUSION AND UNCOATING IN CYTOPLASM

    • GENOME RNA ACTS AS mRNA AND IS TL BY
    • RIBOSOMES IN CYTO INTO PROTEIN (CLEAVED BY PROTEASES)

    MEMBRANE-ASSOC. REPLICATION

    VIRION MORPHOGENESIS IN IC VESICLES; VIRION TRANSPORT AND GLYCOPROTEIN MATURATION; VESICLE FUSION WITH PM AND RELEASE

    d. DIAGNOSIS BY ISOLATION OF VIRUS FROM BRAIN TISSUE,ETC. OR BY DETECTION OF AB IN CSF

    e. NO ANTIVIRAL THERAPY OR VACCINE (SCREEN DONATED BLOOD FOR WNV)
  77. ARBOVIRUSES THAT CAUSE ENCEPHALITIS
    WN - CROWS, FLAVI

    EASTERN EQUINE ENCEPH - BIRDS; MOST SEVERE WITH 50% FATALITY, 5 CASES PER YR

    WESTERN EQUINE ENCEPH- BIRDS - NO RECENT CASES

    ST. LOUIS ENCEPH (FLAVI) - SPARROWS URBAN AREAS. 10-30 CASES PER; FLAVI

    CALIF ENCEPH - RODENTS, 40-80 CASES PER
  78. DENGUE FEVER
    FLAVI

    (+)ssRNA; ENV; ICOSA

    a. NOT ENDEMIC TO US; IN TROPICAL AREAS

    b. AEDES MOSQUITO AS VECTOR

    • c. CLASSIC DENGUE-SUDDEN FLU-LIKE SX WITH FEVER, MALAISE, COUGH, HEADACHE; SEVERE JOINT AND MUSCLE PAIN (BREAKBONE), ENLARGED LN’S, PETECHIAL RASH; SX USUALLY REGRESS
    • AFTER ABOUT A WEEK

    d. DENGUE HEMORRHAGIC FEVER-MORE SEVERE WITH HIGHER FATALITY; INITIAL LIKE CLASSIC DENGUE THEN SHOCK AND HEMORRHAGE IN GI AND SKIN (INCREASED VASCULAR PERMEABILITY AND DROP IN BLOOD PRESSURE AND BLOOD VOLUME); MAY SEE PLEURAL EFFUSION

    DENGUE SHOCK SYNDROME-CROSS-REACTING AB AT TIME OF 2ND INFECTION THAT FORMS AG-AB COMPLEXES THAT ACTIVATE A LOT OF COMPLEMENT AND BIND AND ACTIVATE MACROPHAGES (CYTOKINE STORM-MASSIVE INTERNAL BLEEDING AND SHOCK)
  79. TOGA - ARBO
    (+)ssRNA NON-SEG; ENV, ICOSA


    1. EASTERN AND WESTERN EQUINE ENCEPHALITIS VIRUS

    a. EEE CAUSES MOST SEVERE DISEASE

    b. TRANSMITTED BY CULISETA MOSQUITO WITH WILD BIRD RESERVOIR

    c. ENCEPHALITIS CHARACTERIZED BY SUDDEN ONSET OF FEVER, NAUSEA, VOMITING, HEADACHE

    d. CHANGES IN MENTAL STATUS SOON FOLLOW; RAPID DOWNHILL COURSE WITH STIFF NECK, SEIZURES, COMA

    e. IMMUNITY FOLLOWING INFECTION IS LIFE-LONG

    • f.
    • DIAGNOSIS MADE BY VIRAL ISOLATION OR
    • DETECTING RISE IN AB TITER

    g. NO ANTIVIRAL THERAPY; KILLED VACCINE ONLY FOR HORSES

    COLORADO TICK FEVER VIRUS
  80. EBOLA/MARBURG
    FILOVIRUS FAMILY

    (-)ssRNA LINEAR NON-SEG, ENV

    LONG FILAMENTOUS STRUCTURE

    HELICAL

    CAUSE HEMORRHAGIC FEVER

    1. BEGINS WITH FEVER, HEADACHE, VOMITING, DIARRHEA

    2. BLEEDING INTO GI TRACT

    3. SHOCK AND DISSEMINATED INTRAVASCULAR COAGULATION

    4. TRANSMISSION BY BATS (?) OR SECONDARY TRANSMISSION BY PATIENT’S BLOOD OR SECRETIONS

    5. FATAL BECAUSE OF CYTOKINE STORM OF TNF-ALPHA, IL-6, IL-8; ATTACK ON ENDOTHELIUM, AND EVENTUAL VASCULAR INSTABILITY AND COLLAPSE

    LYMPHOCYTES KILLED AND AB RESPONSE RENDERED INEFFECTIVE

    DIAGNOSIS BY ISOLATION OF VIRUS OR DETECTING RISE IN AB TITER

    NO ANTIVIRAL THERAPY; VARIABLE RESULTS WITH IMMUNE SERUM GLOBULIN

    PREVENTION BY LIMITING SECONDARY SPREAD BY PROPER HANDLING OF PATIENT’S SECRETIONS AND BLOOD; NO VACCINE
  81. ORTHOPOXVIRUSES
    BRICK-SHAPED PARTICLES

    LINEAR DSDNA, A DISK-SHAPED CORE WITHIN A DOUBLE MEMBRANE, AND A LIPOPROTEIN ENVELOPE

    LARGE AND VERY COMPLEX, INDUCING BOTH SPECIFIC AND CROSS-REACTING AB’S

    FAMILY CONSISTS OF THREE VIRUSES:

    1. VARIOLA (SMALLPOX) VIRUS

    a. LIFE CYCLE

    PENETRATION OF CELL AND UNCOATING

    VIRION DNA-DEP. RNA POL. SYNTHESIZES EARLY NON-STRUCTURAL MRNA THAT IS TL IN THE CYTO TO PROTEIN (ENCODE PROTEINS NECESSARY FOR REPLICATION)

    VIRAL REPLICATION IN THE CYTOPLASM

    • LATE GENES EXPRESSED AFTER GENOME IS
    • REPLICATED AND ENCODE STRUCTURAL PROTEINS

    VIRION ASSEMBLES IN THE CYTO AND MOVES TO PM BY ACTIN FILAMENTS (RELEASE AND ACQUIRE ENVELOPE BY BUDDING)

    b. ROUTE OF INFECTION

    TRANSMITTED BY RESPIRATORY AEROSOL OR DIRECT CONTACT WITH LESIONS OR ON FOMITES SUCH AS BEDDING

    • VIRUS INFECTS URT>LOCAL LN’S>BLOOD
    • (PRIMARY VIREMIA)>INTERNAL ORGANS>BLOOD (SECONDARY VIREMIA)>SKIN

    c. SYMPTOMS AND HALLMARKS OF DISEASE

    INCUBATION PERIOD ABOUT 7-14 DAYS

    SUDDEN ONSET OF PRODROMAL SX SUCH AS FEVER AND MALAISE

    SX FOLLOWED BY RASH-VIRAL REPLICATION IN SKIN AND DAMAGE BY CTL KILLING OF VIRALLY-INFECTED CELLS (RASH WORSE ON FACE AND EXTREMITIES-CENTRIFUGAL)

    RASH PASSES THROUGH STAGES FROM MACULES TO PAPULES, VESICLES, PUSTULES, AND CRUSTS AFTER 2-3 WKS

    d. PRINCIPLE HOST DEFENSE

    AB AGAINST VIRUS PROVIDES LIFE-LONG IMMUNITY

    e. DIAGNOSIS

    GROWING VIRUS IN CELL CULTURE

    DETECTING VIRAL AG IN VESICULAR FLUID BY IMMUNOFLUORESCENCE

    TREATMENT

    NO ANTIVIRAL THERAPY

    g. PREVENTION

    LIVE, ATTENUATED VACCINE WITH VACCINIA VIRUS GIVEN INTRADERMALLY

    FORMATION OF VESICLE INDICATES SUCCESS

    AN EXPOSED INDIVIDUAL CAN BE IMMUNIZED AS LONG AS 4 DAYS AFTER EXPOSURE AND BE FINE

    • VACCINIA IMMUNE GLOBULINS USED FOR
    • COMPLICATIONS (ENCEPHALITIS, GENERALIZED VACCINIA, ETC.)

    CONTRAINDICATIONS FOR VACCINATION: ECZEMA, ATOPIC DERMATITIS, OTHER ACUTE, CHRONIC, OR EXFOLIATIVE SKIN CONDITIONS; PREGNANCY, IMMUNODEFICIENCY OR SUPPRESSION

    h. INTERESTING FACTS ABOUT VIRUS

    REPLICATION IN THE NUCLEUS

    ERADICATED IN 1979 BECAUSE OF ADVENT OF VACCINE

    GOOD VACCINE:

    1. HUMANS ARE ONLY RESERVOIR

    2. DISEASE IS RECOGNIZED EASILY FOR PURPOSES OF VACCINATION OR QUARANTINE

    3. ACUTE INFECTIONS RESULT IN EITHER DEATH OR LIFE-LONG IMMUNITY (NO CARRIER STATE)

    4. VACCINIA VIRUS IS HIGHLY IMMUNOGENIC AND MINIMALLY PATHOGENIC (EFFECTIVE VACCINE)

    IMMUNE EVASION BY ENCODING PROTEINS (“VIRORECEPTORS”)-RECEPTORS FOR MAJOR CYTOKINES TGF-BETA, IFN-GAMMA, IL-1, AND COMPLEMENT –INHIBIT CYTOKINES
  82. VACCINIA VIRUS
    ORTHOPOX

    BRICK/DUMBBELL; COMPLEX

    ldsDNA; REP IN CYTO

    a. VIRTUALLY NON-PATHOGENIC FOR HUMANS

    b. USED FOR STUDIES ON POXVIRUS REPLICATION AND USED TO MAKE VACCINE

    c. DEMONSTRATES SIGNIFICANT RESISTANCE TO EFFECTS OF IFN
  83. POXVIRUS OF ANIMAL ORIGIN
    BRICK OR DUMBBELL-SHAPED

    lcdDNA; REP IN CYTO

    a. TRANSMITTED BY CONTACT WITH INFECTED ANIMALS (BITE OR CONTACT WITH LESIONS OR BODY FLUIDS)

    b. COWPOX-VESICULAR LESIONS ON UDDERS OF COWS; SIMILAR LESIONS ON PPL WHO MILK COWS

    c. ORF VIRUS-CAUSE OF CONTAGIOUS PUSTULAR DERMATITIS IN SHEEP AND VESICULAR LESIONS IN SHEEPSHEARERS

    • d. MONKEYPOX-DISEASE OF MONKEYS AND RODENTS IN CENTRAL AND WEST AFRICA; BEGINS WITH FEVER, HEADACHE,
    • MUSCLE ACHES, SWOLLEN LN’S, ETC.; 1-3 DAYS AFTER FEVER, PAPULAR RASH APPEARS AND MAY BECOME VESICULAR (ILLNESS LASTS 2-4 WKS)

    DISEASE CAN ALSO BE SPREAD PERSON-TO-PERSON (RESP. DROPLETS OR CONTACT WITH INFECTED BODY FLUIDS)

    TESTS INCLUDE PCR-BASED ASSAY, EM, GENE SEQUENCING, IMMUNOHISTOCHEM, SEROLOGIC

    NO PROVEN TX; SMALLPOX VACCINE REDUCES RISK (NO RECOMMENDATION FOR PRE-EXPOSURE VACCINE)
  84. RUBELLA
    1. TOGAVIRUS FAMILY

    2. (+)ssRNA, NON-SEG, ENV, ICOSA, E1 AND E2 SPIKES

    LIFE CYCLE

    1. ATTACH TO CELL SURFACE VIA SPECIFIC RECEPTORS AND ENTER HOST CELLS VIA ENDOCYTOSIS

    • 2. ACIDIFICATION OF ENDOSOME RESULTS IN FUSION OF VIRAL ENVELOPS WITH ENDOSOME AND RELEASE OF
    • VIRION

    • 3. WHEN RELEASED FROM CAPSID, IMMEDIATE PRODUCTION VIA HOST CELL
    • POL OF NON-STRUCTURAL PROTEINS, MADE AS ONE BIG PROTEIN AND CUT INTO FRAGMENTS, INCLUDING VIRAL RNA POL. (REPLICASE)

    4. TC/TL OF LATE PROTEINS INTO ONE BIG PROTEIN AND CUT INTO E1, E2, AND CAPSID

    5. ASSEMBLY AND BUDDING OF NEW VIRIONS

    ROUTE OF INFECTION

    1. TRANSMITTED BY RESPIRATORY DROPLETS AND FROM MOTHER TO FETUS

    2. INITIAL REPLICATION IN NASOPHARNYX AND LOCAL LN’S>BLOOD>INTERNAL ORGANS AND SKIN (RASH)

    SYMPTOMS AND HALLMARKS OF DISEASE

    1. RUBELLA

    a. MILDER, SHORTER DISEASE THAN MEASLES

    b. INCUBATION PERIOD OF 14-21 DAYS; BRIEF PRODROMAL PERIOD OF FEVER AND MALAISE FOLLOWED BY MACULOPAPULAR RASH (PROGRESSES DOWNWARD)

    c. RASH TYPICALLY LASTS 3 DAYS

    d. POLYARTHRITIS CAUSED BY IMMUNE COMPLEXES IN ADULTS (ESP. WOMEN)

    2. CONGENITAL RUBELLA SYNDROME

    a. NON-IMMUNE PREGNANT WOMAN IS INFECTED DURING 1ST TRIMESTER (WORST TIME BECAUSE ORGANS ARE DEVELOPING)

    • b. COMMON DEFECTS INCLUDE: DEAFNESS, EYE ABNORMALITIES LIKE CATARACTS, CONGENITAL HEART
    • DISEASE (PATENT DUCTUS ARTERIOSUS), LOW BIRTH WEIGHT, MICROCEPHALY, ETC.

    c. MECHANISM UNKNOWN; RUBELLA VIRUS ABLE TO INDUCE APOPTOSIS IN CELLS THAT MIGHT BE CONNECTED WITH P53

    PRINCIPLE HOST DEFENSE

    1. NATURAL INFECTION PROVIDES LIFE-LONG IMMUNITY

    2. MATERNAL AB (IGG!) CROSSES PLACENTA AND PROTECTS NEWBORN

    DIAGNOSIS

    1. GROWN IN CELL CULTURE (MEASURE ABILITY TO INTERFERE WITH ECHOVIRUS CPE)

    • 2. FOUR-FOLD OR GREATER RISE IN AB TITER BETWEEN ACUTE AND CONVALESCENT SERA IN ELISA OR
    • HA INHIBITION

    • 3. PRESENCE OF AB IN PREGNANT WOMAN: IGM IS RECENT INFECTION AND IGG INDICATES IMMUNITY AND
    • PROTECTION OF BABY

    TREATMENT

    1. NO ANTIVIRAL THERAPY

    PREVENTION

    • 1. IMMUNIZATION WITH LIVE, ATTENUATED VACCINE-GIVEN SUBCUTANEOUSLY AT 15 MONTHS (IN COMBINATION WITH MEASLES AND MUMPS) AND TO UNIMMUNIZED YOUNG ADULT WOMEN IF THEY ARE NOT
    • PREGNANT AND WILL USE CONTRACEPTION FOR NEXT 3 MONTHS

    INTERESTING FACTS ABOUT VIRUS

    1. CAUSES SEVERE MALFORMATIONS IN FETUS, ESPECIALLY DURING 1ST TRIMESTER
  85. PARVO
    1. PARVOVIRUS

    2. SMALL NON-ENV WITH (-)ssDNA; ICOSAHEDRAL CAPSID (ONLY ONE SEROTYPE)

    LIFE CYCLE

    1. AFTER ADSORPTION TO HOST CELL RECEPTORS, VIRION PENETRATES AND MOVES TO NUCLEUS, WHERE REPLICATION OCCURS (PENETRATION MEDIATED BY PHOSPHOLIPASE A2 ACTIVITY CARRIED ON AMINO-TERMINAL PEPTIDE OF CAPSID VP1)

    2. NON-STRUCTURAL, REPLICATION, STRUCTURAL PROTEINS

    3. SINGLE-STRANDED DNA HAS HAIRPIN LOOPS AT BOTH ENDS THAT PROVIDE AREAS TO INITIATE REPLICATION

    4. VIRAL MRNA SYNTHESIZED BY CELLULAR RNA POLYMERASE FROM dsDNA INTERMEDIATE

    5. PROGENY VIRIONS ASSEMBLED IN NUC

    6. RELEASE BY CELL LYSIS

    ROUTE OF INFECTION

    • 1. TRANSMITTED PRIMARILY BY RESPIRATORY ROUTE, TRANSPLACENTAL, AND BLOOD TRANSFUSIONS (HUMANS
    • ARE NATURAL RESERVOIR)

    2. VIRUS INFECTS RBC PRECURSORS (ERYTHROBLASTS) IN BONE MARROW, CAUSING APLASTIC ANEMIA, AND ENDOTHELIAL CELLS IN BLOOD VESSELS, CAUSING RASH

    SYMPTOMS AND HALLMARKS OF DISEASE

    1. ERYTHEMA INFECTIOSUM (SLAPPED CHEEK SYNDROME, FIFTH DISEASE)

    a. MILD DISEASE PRIMARILY IN CHILDHOOD CHARACTERIZED BY BRIGHT RED RASH, PRIMARILY ON THE CHEEKS, AND FEVER, RUNNY NOSE, AND SORE THROAT

    b. “LACY” RASH ON BODY

    c. SX RESOLVE IN ABOUT A WEEK

    d. FIFTH DISEASE OF MACULOPAPULAR RASH IN CHILDHOOD (OTHER FOUT ARE MEASLES, RUBELLA, SCARLET FEVER, AND ROSEOLA)

    2. APLASTIC ANEMIA

    a. REALLY AFFECT CHILDREN WITH CHRONIC ANEMIA LIKE SICKLE CELL ANEMIA

    3. FETAL INFECTIONS

    a. FETAL DEATH DURING 1ST TRIMESTER

    b. HYDROPS FETALIS DURING 2ND SEMESTER

    MASSIVE EDEMA OF FETUS SECONDARY TO CHF FROM SEVERE ANEMIA BY B19-KILLED ERYTHROBLASTS

    c. NO IMPORTANT CLINICAL FINDINGS DURING 3RD TRIMESTER

    4. ARTHRITIS

    a. IMMUNE COMPLEXES OF VIRUS AND IGM OR IGG CLOGGED IN SMALL JOINTS OF FEET AND HANDS BILATERALLY

    b. MOSTLY IN WOMEN

    5. CHRONIC B19 INFECTION

    a. PEOPLE WITH IMMUNODEFICIENCY (AIDS, TRANSPLANT, ETC)

    PRINCIPLE HOST DEFENSE

    1. AB (IGM, IGG) PROVIDE LIFE-LONG IMMUNITY

    DIAGNOSIS

    1. FIFTH DISEASE AND APLASTIC ANEMIA BY DETECTING IGM AB

    2. B19 ISOLATION FROM THROAT SWABS (NOT USUALLY DONE)

    3. VIRAL DNA IN BLOOD OR AMNIOTIC FLUID BY PCR

    TREATMENT

    1. NO SPECIFIC TX
  86. MOLLUSCIPOX
    ORTHOPOX

    BRICK/DUMBBELL; COMPLEX

    ldsDNA

    2. MOLLUSCUM CONTAGIOSUM VIRUS-BENIGN EPIDERMAL TUMOR

    • a.
    • FLESH-COLORED PAPULE ON SKIN OR MUCOUS MEMBRANE THAT IS PAINLESS,
    • NON-PRURITIC, AND NOT INFLAMED (UMBILICATED/ CUP-SHAPED CRATER WITH
    • WHITE CORE)-SELF-LIMITING BUT CANLAST FOR MONTHS

    b. LESION COMPOSED OF HYPERPLASTIC EPITHELIAL CELLS WITH EOSINOPHILIC INCLUSION BODY INSIDE (CONTAINS PROGENY MCV)

    c. TRANSMITTED BY CLOSE PERSONAL CONTACT, INCLUDING SEXUALLY, AND INDIRECT CONTACT (SHARING TOWELS, CLOTHING)

    d. DISEASE COMMON IN CHILDREN, CAUSING LESIONS AROUND EYES AND ON TRUNK (ADULT LESIONS IN GENITAL AREA-MORE INFLAMED)

    e. LESIONS CAN BE WIDESPREAD IN PPL WITH LOW CMI RISING CASES AS STD AND IN AIDS PTS

    g. VIRUS IS POOR IMMUNOGEN; ABOUT 1/3 OF PTS. NEVER PRODUCE AB’S AGAINST IT AND CAN GET SUBSEQUENT INFECTIONS

    • h. DIAGNOSIS MADE CLINICALLYREMOVAL
    • OF LESIONS BY CURETTAGE OR LIQUID NITROGEN

    NO ANTIVIRAL THERAPY; CIDOFOVIR AND HAART MAY HELP IN IMMUNOCOMPROMISED PTS; NO VACCINE
  87. ARENAVIRUS
    ZOONOTIC

    2X (-)ssRNA; ENV, HELICAL CAPSID

    LASSA FEVER VIRUS-HEMORRHAGIC FEVER

    LYMPHOCYTIC CHORIOMENINGITIS VIRUS-ASEPTIC MENINGITIS

    c. MINOR VIRAL PATHOGENS

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