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46 Cards in this Set
- Front
- Back
Arthropod-Borne Encephalitis Viruses
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- from inf birds/rodents to humans via mosquito bite
- must replicate in mosquito gut then move to salivary gland prior to transmissions - peak is mid to late summer - no human to human spread - human viremias insufficient to let humans be the reservoir - Alphavirus genus of the family Togaviridae and the Flaviviridae family |
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Alphaviruses Types
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- *Eastern Equine Encephalitis (EEE)*
- Western Equine Encephalitis (WEE) - Venezuelan Equine Encephalitis (VEE) |
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Flaviviruses Types
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- *St. Louis Encephalitis (SLE)*
- Japanese Encephalitis (JE) - Tick-Borne Encephalitis (TBE) - West Nile virus - Dengue virus |
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Alphavirus Structure and Replication
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- Togaviridae family
- (+) sense ssRNA - Icosahedral nucleocapsid(1 capsid protein) - envelope w/ 2 viral prots(M and E) - Replication in cytoplasm with budding at PM |
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Alphavirus Epi (EEE)
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- wild birds resivour(amplifying host)
- mosquito persistently infected - along eastern seaboard - only a few cases a year, only 2% is Ab + in epidemics - Aedes albopictus, “Asian tiger mosquito”, is new - might let virus be a bigger problem, since it can feeds on birds and humans - human-to-human in aerosol in lab |
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Alphavirus Clinical Features
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- Most subclinical effected by:
a)manner of inoculation b)non-specific immunity(old/kids=more effect) c)diff in host immunity(degree of immune-mediated damage) d)strain differences among viruses - febrile illness, may lead to encephalitis (50-75% fatal) - 10-12 day febrile illness, then fever, stiff neck, loss of consciousness - may go to seizures, coma and death or it may resolve |
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Alphavirus Pathogensis
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- moves from the blood ⇒ endothelial cells ⇒ nerve cells
- symptoms from viral action on nerve cells and host imflam response - EEE is cytolytic(inf-induced apoptosis) - IFNs important |
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Alphavirus Treatment and Diagnosis
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- recovery due to development of Ab to envelope glycoproteins
- diagnosed by presentation or w/ serological tests like IgM ELISA - No vaccine or treatment |
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Flaviviruses Structure and Replication
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- Flaviviridae family, like HCV
- can cause yellow fever - (+) sense ssRNA - Icosahedral nucleocapsid w/ 1 capsid protein w/ envelope (M and E) - Replication in cytoplasm with budding at internal membranes |
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Alphaviruses Immunity
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- Protective humoral immunity directed to envelope proteins
- CTLs do inflam response |
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Flaviviruses Immunity
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- Protective humoral immunity directed to envelope proteins
- CTLs do inflam response |
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St. Louis Encephalitis Virus Clinical Features
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- most prevalent arthropod encephalitis viruses in US
- most subclinical - may begin w/ fever, malaise, headache, drowsiness -> encephalitis, meningitis, & febrile headache - elderly=10x more likely to die than young, have more severe symptoms often complicated by pre-existing conditions |
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SLE Virus Epi
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- maintained in mosquitoes in winter reservoirs in North Am
- transmission begins in spring/early summer w/ birds as amplifying host - human disease peaks from July - Sept - 50/year in US - 5-15 year outbreak cycles |
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St. Louis Encephalitis Virus Diagnosis
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- consider if encephalitis, meningitis or febrile headache in July-September, esp old
- PCR of blood, CSF or tissue - IgM in serum or CSF by ELISA - Ab testing of paired(acute/convalescent) sera - immunofluor for SLE Ag in cells of urine sediment or CSF |
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St. Louis Encephalitis Virus Treatment and prevention
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- no vaccine, treatment limited to supportive therapy
- reduce of vector populations - hard to do since expansion of mosquito habitat, insecticide resistance, new vectors species, reduction in mosquito control programs |
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West Nile Virus
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- severe meningoencephalitis in elderly in israel
- came to US in 1999(plane), found in wild birds, horses and humans - 2002 outbreak, most cases from mosquito bite, some from transplants - blood is now screened - usually in old - if pregnant, rarely associated with spontaneous abortion and neonatal illness, but not birth defects - but intrauterine infection possible |
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The Picornaviridae family
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1)Genus Enterovirus:
a) poliomyelitis virus b) echoviruses (enteric cytopathic human orphan virus) c) enteroviruses d) coxsackieviruses (Coxsackie, NY …site of first isolation) 2)Genus Rhinovirus (including “cold” viruses) 3)Genus Hepatovirus (hepatitis A virus) |
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Poliomyelitis Structure
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- small, (+) ssRNA
- spherical, icosahedral, acid stable(suvive at pH 3 or lower) - 3' poly (A) tail and a 5’ VPg - NTRs flank coding regions |
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Poliomyelitis Replication
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- initially replicates in the human intestinal tract
- attaches to receptors (which determine tropism) - viropexis(Receptor mediated Endocyt) does penetration and uncoating(energy-dependant) - translation is cap-independent - cap-binding complex (CBC) shuts of host proteins - uses RNAdependentRNA polymerase - asymmetric, many (+) molecules made few (-) |
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Poliomyelitis Clinical Features
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- most subclinical(99%)
- malaise, fever, headache, nausea(only last a few days->"abortive poliomyelitis" - rarely can cause aseptic meningitis (resolves in 2-10 days) - rarely, paralytic polio - most significant paralysis presents w/in a few days, and most recovery is w/in 6 months - “progressive post-poliomyelitis muscle atrophy” - 25-40% have additional deterioration decades later from effects of aging |
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Poliomyelitis Pathogenesis
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- alimentary tract via mouth
- shed in feces for several weeks - 1o replication in OP mucosa, tonsils, LNs - ingested to gut and adjacent lymphoid tissue - 1o viremia from infection of Peyer's patches and mesenteric LNs - spread to SC, meninges, and muscle - paralysis after 10 days from: direct destruction of the neurons or edema-induced damage of the neurons (reversible) - fatal outcome if infection gets the CV and Resp centers of the medulla oblongata |
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Poliomyelitis Epidemiology
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- poliomyelitis not endemic (unlike other enteros) b/c of vaccination
- bad(endemic) in Sub-Saharan Africa and South Asia - in US, only in immunocompromised vaccinees, imports, vaccinated contact |
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Non-poliomyelitis enteroviruses Epidemiology (NPEV)
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- usually no pandemic, just periodic sweeping every few years
- most mild or asymptomatic - usually in kids in summer - lower socioeconomic areas - often found shellfish harvesting water |
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Poliomyelitis Diagnosis
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- clinical signs nondescript, unless combined w/ knowledge of a current epidemic
- specific viruses identified via immuno-serological techniques - appropriate specimens are stools, rectal and throat swabs - mixed infections of enteroviruses are not common |
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Poliomyelitis Prevention and Treatment
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- vaccination is key (but none for other enteroviruses)
- isolation of infected - resistant to disinfectants |
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Poliomyelitis Killed(Salk, IPV) vaccine advantages
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- can be combined w/ (DPT)
- no mutation - ok if immunodeficient - reduces spread of live polioviruses |
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Poliomyelitis Killed(Salk, IPV) vaccine disadvantages
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- low % develop Abs, so repeated boosters needed
- no intestinal immunity - expensive |
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Poliomyelitis Live(Sabin, OPV) polio vaccine advantages
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- humoral and intestinal immunity (like natural)
- immunity lifelong - oral, works quickly - relatively inexpensive - uses of continued cell lines, no contaminants |
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Poliomyelitis Live(Sabin, OPV) vaccine disadvantages
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- may mutate -> neurovirulence
- spreads to other persons and environment - problem if immunodeficient - monkey testing |
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Polyomaviruses JC virus
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- PML, a progressively fatal, neurodegenerative disease
- due to SV 40 ('the vacuolating agent') – maybe from contaminated OPV vaccine - Inclusion bodies seen in brain - 1-10% of AIDS patients |
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Polyomaviruses BK virus
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- isolated from urine of pt after renal transplant
- in 50% of patients after bone marrow transplantation - distantly related to SV 40 |
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Polyomaviruses Structure
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- Papovavirus family
- naked, icosahedral virions - circular dsDNA - from SV40 - in 40% of tumors in non-Hodgkins lymphomas and brain and bone tumors and mesotheliomas – contaminated polio vaccine? |
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Polyomaviruses Replication
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- replicate in nucleus
- do NOT encode a viral DNA dependent DNA polymerase; - use host DNA dependent DNA polymerase for genome replication - uses host DNA dependent RNA polymerase II for transcription - progeny virions assemble in cell nucleus |
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Polyomaviruses Pathogenesis
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- only in immunosuppressed -> inapparent, cryptic infection
- transmitted via respiratory route - host cells are killed by viral cytolytic infection - cannot manifest transformation phenomenon - can be transformed to neoplastic growth in non-natural cells |
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Herpesviridae family
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- herpes simplex (HSV)
- varicella zoster virus (VZV) - cytomegalovirus (CMV) - Epstein-Barr virus (EBV) - HHV 6 and HHV 7 (roseola) - HHV 8 (Kaposi sarcoma associated virus) - monkey B virus (serious neurotropic virus for humans) |
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HSV-1 Clinical Features
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1)Primary Disease usually asymptomatic (esp if < 10yr)
- if symptoms, gingivostomatitis, with vesicular eruptions on mouth -> ulcerative lesions - 2-3 weeks 2)latent infection in sensory neurons then reactivated disease from stress - prior to episode, often altered sensation of area(pain,itch,tingle) then vesicls 1-2 days later – fewer lesions than 1o and on mucocutaneous borders - asymptomatic shedding common |
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HSV-2 Clinical Features
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1)Primary Disease usually symptomatic
- painful, vesicular lesions on the genitals -> pustules and ulcers - systemic infection common 2)reactivated Disease is milder - If 1o was severe, recurrences more frequent - asymptomatic shedding common |
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HSV in Pregnancy Clinical Features
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- vertical transmission of HSV-2 during delivery (asymptomatic shedding)
- recurrent disease is much less risky because of the reduced shedding of the virus - in utero cases systemic, with high mortality |
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HSV Acute Necrotizing Encephalitis
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- HSV=most common cause, high mortality, sporadic encephalitis
- usually in immunocompromised |
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Herpes simplex Keratoconjunctivitis
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- second to trauma as a cause of corneal blindness in the U.S.
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HSV Structure
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- large dsDNA
- icosahedral capsid surrounded by the tegument in envelope |
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HSV Replication
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- in nucleus
- transcription by host DNA dependent RNA polymerase II - replication by virus-coded DNA dependent DNA polymerase - envelope and maturation in cytoplasm |
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HSV Pathogenesis
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- invades epi -> multinucleate giant cells
- released via exocytosis and cell necrosis - main pathogenic effect is cell lysis: 1)leaks vesicular fluid between the dermis and epidermis->creating the vesicle->facilitates spread |
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HSV Epi
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- HSV-1 universal, usually before 5
- spread by direct contact with lesions or secretions - asymptomatic kids are major HSV-1 source - no animal vectors or seasonal patterns - sex is HSV-2 source – 20% of females shed asymptomatically |
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HSV Diagnosis
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- history and vesicular lesions
- characteristic CPE in tissue culture - in herpes encephalitis, PCR of the CSF |
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HSV Treatment
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- no vaccine for either form is yet licensed
- acyclovir (Zovirex™), a nucleoside analog – only active in virus-infected cells -> chain termination - can become resistant from mutations of viral TK that don’t accept ACV - fortunately, acyclovir resistant mutants are avirulent - a new subunit vaccine of HSV-2 envelope D is in trial |