Virology Flashcards
HPV (oncogenesis)
Localized infection - skin warts
Oncogenic: via E6 disabling host Rb and E7 acting on host’s p53
*can cause squamous cell carcinoma of cervix
Lysogenic (Temperate) Virus
Lysogenic cycle - host cell multiplies and daughter cells contain the prophage
Lytic (Virulent) Virus
Kills host immediately; particles released by host cell lysis or budding
EBV (oncogenesis and evasion mechanism)
Receptor: CR2
Cell: B cell
Evasion: produces IL-10 (anti-inflamm. cytokine)
*silent sub-clinical virus
HIV (tropism)
Receptor: CD4 (plus CCR5 and CXR4 on macrophage)
Cell: Th and Macrophages
Influenza A (tropism)
Receptor: Sialic acid (Neuraminidase on virus breaks down sialic acid in order for aggregated virions to bud out of the cell)
Cell: epithelial cell
Rabies (tropism and inclusions)
Receptor: nicotenic ACh Cell: neurons Inclusions: Negri bodies Mechanism: retrograde, affects CNS eventually "slow virus"
Viral Attachment Proteins (VAP)
Viral glycoproteins located on the outer leaflet (envelope for enveloped viruses OR the capsid for naked viruses)
*contributes to the viral “tropism”
RNA Dependent RNA-Pol (RNA Replicase)
Group IV codes for RR, Group III and V code for RR and also contains the enzyme in their virion
Antigenic Drift
Small change in a genome w/in specific strain, happens at slow rate compared to Ag Shift
*type of antigenic variation (e.g. - orthomyxo specifically influenza virus)
Antigenic Shift
Mix and match of chromosomes btwn 2 diff strains of virus - faster change than drift
*reassortment of genome (type of antigenic variation)
Phenotypic Mix
Genome of 1 virus is coated w/ proteins from another viral genome mixed w/ capsid from another virus
Viremia
Transmission of virus by blood throughout the entire body reaching distant organs
Paralytic Poliomyelitis
Fecal-oral path w/ initial propagation in SI followed by viral reach to mesenteric lymph nodes
- initial viremia bloodstream brings virus to some organs
- secondary viremia brings virus to CNS
- IgG produced
Incubation Period
Pt is asymptomatic (virus enters host cell and is not detectable)
Prodromal Period
Non-specific sx’s present
Specific-illness Period
Specific sx’s signature of certain viral dz
Recovery Period
Healing of dz, or can move into chronic state or cause infection at a secondary site
Congenital Rubella
ROS: cataracts, patent ductus arteriosus (PDA), intellectual disability, microcephaly, deafness
*transplacental transmission
Cytomegalovirus (CMV)
Inclusions: “owl’s eye” in nucleus
Evasion: blocks MHC-I being presented
*can be transmitted trans-placental or breastfeeding
(Most common viral cause of death in BMT pt’s)
Virus eradicated by vaccine?
Smallpox
Type I Hypersensitivity
Mediator: IgE and vasoactive mediators (mast cell degranulation)
Benefits: anti-parasitic responses and toxin neutralization
Pathologic effects: localized allergies, systemic anaphylaxis
Microbes involved in Pulmonary Type I Hypersensitivity
Molds: leads to asthma
G-ve: leads to organic dust toxic syndrome or Asthma
Type II Hypersensitivity
Mediator: IgG w/ Ag
Mechanism: complement mediated cytotoxicity, or modification of cell surface receptor function
Benefit: lysis/phagocytosis of extracellular microbes
Pathologic effect: RBC destruction, tissue damage
Examples of Type II Hypersensitivities
Infectious cause: Guillan-Barre, Dengue and Zika, CMV (HHV-5)
Ag mimicry: acute RF following strep throat infection, RBC lysis due to ABO incompatibility
Drug induced: penicillin allergy
Type III Hypersensitivity
Mediator: IgG w/ soluble Ag (immune complex)
Mechanism: complement activation
Benefit: acute inflamm @ site of extracellular microbes
Pathologic effect: Arthus rxn, serum sickness and generalized drug rxn’s
Infectious cause of Type III Hypersensitivity
Staph infective endocarditis, strep glomerulonephritis, Arthus Rxn, Serum Sickness-like post-infectious Rxn (viral infections)
*SLE and RA
Type IV Hypersensitivity
Mediator: Cell-mediated, Ab independent
Mechanism: phagocytized soluble ag presented to CD4+ T cells activates macrophages and inflammation
Benefit: protects against fungi, intracellular bacteria and viruses
Pathologic effect: acute - contact dermatitis, Tb skin test; chronic - granuloma formation
Granuloma
Aggregate of cells aiming to wall-off and isolate structures that cannot be otherwise killed/expelled
E.g. - TB, leprosy, schistosomiasis, sarcoidosis and Crohn’s dz
C5-C9 deficiency
Present with recurrent Neisseria infections (MAC can’t form)
Titer
Amount of dilution of virus until no hemagglutination occurs (and the RBCs sediment in the bottom)
Hepatitis D Virus (HDV)
Satellite virus, requires HBV as helper virus
Cell entry: requires HD antigen from HDV and HB antigen from HBV to allow host cell entry
Eclipse phase
After initial infection the viral particles enter host cells so they “disappear”, this is the latent period until new visions are assembled (which is done by self-assembly)
Early Proteins
Responsible for initial behavior of the virus and prep for replication of viral nucleic acid (non-structural proteins)
Late Proteins
Participate in formation of the viral capsomeres such as structural proteins
HCV and HIV drug targets
Viral proteases as targets
Latent Viral Infection
Varicella-Zoster (HHV3) presents as chicken pox (varicella) but in secondary presents as herpes zoster aka shingles
*trigeminal or thoracic ganglion
Latency in HSV-1
Resides in trigeminal ganglion, the first/acute infection is worse
*reactivation by UV, stress, illness and the sores are not as bad as the first time
Chronic Viral Infection
HBV and HCV - can lead to HCC eventually
Silent Subclinical Viruses
Life-long infection
E.g. - CMV and EBV
Slow Infections
Long incubation period effort dz presentation
E.g. - JC virus and prions
JC Virus
Family: polyoma
Dz: can present as Progressive Multifocal Leukoencephalopathy (PML)
BK Virus
Family: polyoma
Dz: BK nephropathy
Measles (latency)
Aka German Measles
Family: paramyxo
Dz: Subacute Sclerosing Panencephalitis (SSPE)
Latency: 1-10 years
Rubella (latency)
Family: toga
Dz: Progressive Rubella Panencephalitis
Latency: 10-20 years
HIV (latency)
Family: retro
Dz: AIDS
Latency: 5-10
Rabies (latency)
Family: rhabdo
Dz: rabies
Latency: 3-12 weeks
*Negri bodies inclusions in neuron cytoplasm
HTLV (latency)
Family: retro
Dz: leukemia/lymphoma of T cells
Latency: 10-30 years
Syncytial Formation
Instead of killing host cell, virus stimulates host cell to fuse with other cells leading to multinucleated giant cells (syncytia)
E.g. - paramyxo (RSV, measles, mumps), HSV-1, HSV-2, HIV
Rotavirus (symptoms)
Mechanism: initiates stimulation of enteric nervous system
ROS: cause diarrhea likely due to excessive cytokine production and fluid release
Arthritis caused by viruses
Early HBV, parvo B19, rubella
Viral Exanthemas
Abrupt appearance of skin rash affecting several areas simultaneously
E.g. - measles, rubella (German measles), parvo B19, HHV-6 and HHV-7
Enanthema
Mucous membrane eruption
Viral Immunopathogenesis (cause)
Attributed to or driven by cytotoxic CD8+ T cells or Ab production
Dengue
Family: flavivirus (4 serotypes)
ROS: high fever, lymphadenopathy, myalgia, pain, HA, maculopapular rash
Complication: hemorrhagic fever due to ADE
*antibody dependent enhancement (ab to a diff serotype enhances the pathogenicity of the new serotype infecting the host)
Ab-Dependent Enhancement (ADE) in Dengue
Initial infection with stereotype 1, and subsequent infection with stereotype 2 the Ab’s will be produced for 1 and only partially block serotype 2
*does not enhance killing but facilitates infection by serotype 2
Oncogenic Viruses
HTLV, HBV, HCV, HPV 16 and 18, EBV, HHV-8
*DNA viruses are more common drivers of tumorigenesis in humans
HTLV-1 (oncogenesis)
Family: retro
Oncogenesis: linked to TAX transactivator gene which works on activating viral transcription and on promoters in terminal viral LTR region
Dz: adult T cell lymphoma
HHV-8 (oncogenesis)
Susceptibility of developing Kaposi Sarcoma when immunocompromised
*most frequent tumor in AIDS pt’s
EBV (HHV-4) …oncogenesis
Oncogenesis: immortalizes B cells by producing a potent B cell nitrogen and by preventing apoptosis
Dz: Hodgkin lymphoma, Burkitt lymphoma, gastric ca, nasopharyngeal carcinoma
Negri Bodies
Inclusion bodies in cytoplasm of nerve cells infected w/ rabies
Owl’s Eyes
Inclusions in nucleus of CMV infected cells
Pox Virus
Structure: complex
Replication: cytoplasm
Inclusions: intracytoplasmic acidophilic inclusions
Evasion: produces decoy receptors
Reovirus (inclusions)
Perinuclear cytoplasmic acidophilic inclusions
Virokines
Viral products that interfere with host cytokine activity
E.g. EBV produces IL-10 (anti-inflammatory cytokine)
HSV
Pathogenesis: initiates apoptosis leading to fragmentation of host genome then cell lysis
Evasion: fucks with TAP transporter
Poliovirus (pathogenesis)
Inhibits cellular Initiation Fator (IF) in protein synthesis in neurons
Adenoviruses
Pathogenesis: round, swollen cells that can climb together
Oncogenesis: through E1A and E1B
Measles
Aka Rubeola
Family: Paramyxo
*“Three C’s”: cough, coryza, conjunctivitis
*Koplik spots: gray-white spots on buccal mucosa
