Virology Flashcards
Adenovirus
DNA Naked Double stranded
Most common cause of TONSILLITIS
•Hemorrhagic cystitis
•Viral conjunctivitis
Transmission: Respiratory droplet, Feco-oral route
Vaccination: Live attenuated
BK Virus
Naked
double stranded
CIRCULAR
Hemorrhagic cystitis
Nephropathy
Transplant patients
JC Virus
Naked
DOUBLE STRANDED
CIRCULAR
Area: Oligodendrocytes
Progressive Multifocal LEUKOEncephalopathy - demyelinating
NON ENHANCING lesions on CT and MRI
CD4 <200
The protein shell, or coat that encloses the nucleic acid genome
Capsid
Morphologic units seen in the electron microscope on the surface of icosahedral virus particles
Capsomeres
A virus particle that is functionally deficient in some aspect of replication
Defective virus
Ex Hepa D
A lipid-containing membrane that surrounds some virus particles
Envelope
The protein nucleic acid complex representing the packaged form of viral genome
Nucleocapsid
The complete virus particle
Virion
Hepatitis B virion
Dane
Modes of Viral Multiplication
The host cell is absolutely necessary for viral multiplication
Multiplication cycles in animal viruses
Adsorption Penetration Uncoating Synthesis Assembly Release
Virus encounters susceptible host cells
Adsorbs specifically to receptor sites on the cell membrane
Because of the exact fit required, viruses have a limited host range
Adsorption
Flexible cell membrane of the host is penetrated by the whole virus or its nucleic acid
Penetration
Entire virus engulfed by the cell and enclosed in a vacuole or vesicle
Endocytosis
Form ofPenetration
The viral envelope can also directly fuse with the host cell membrane
Penetration
Enzymes in the vacuole dissolve the envelope and capsid
The virus is now uncoated
Uncoating
Free viral nucleic acid exerts control over the host’s synthetic and metabolic machinery
DNA viruses enter host cell’s nucleus where they are replicated and assembled
DNA enters the nucleus and is transcripted into RNA
The RNA becomes a message for synthesizing viral proteins (translation)
New DNA is synthesized using host nucleotides
RNA viruses recplicated and assembled in the cytoplasm
Synthesis
Only DNA virus that replicates in cytoplasm
Pox virus
Mature virus particles are constructed from the growing pool of parts
Assembly
Nonenveloped and complex viruses are released when the cell lyse or ruptures
Enveloped viruses are liberated by budding or exocystosis
Anywhere from 3,000 to 100,000 virions may be released, depending on the virus
Entire length of cycle - anywhere from 8 to 36 hours
Release
Stages of Viral Infection in the Cellular Level
Viral interactions with a host’s cell surface
Viral entry into a host cell
Viral gene expression and replication
Viral assembly and release
Only DNA Hepadna virus
Hepa B
Single stranded DNA
Parvoviridae
Circoviridae
Picornaviridae
Polio
Hepatitis A
Bullet-shaped virus
Rhabdoviridae
Crown-shaped spike
Corona virus
Viruses can directly damage host cells by entering them and replicating at the host’s expense
Viruses may inhibit host cell DNA, RNA or protein synthesis
Viral proteins may directly damage host cell’s plasma membrane
Viruses may lyse host cells
Viruses may manipulate programmed cell death
Viruses nay cause malignant transformation
Mechanism of viral injury
Viruses that lead to malignant transformation
Hep B, Hep C
HPV
EBV (NPC, Burkitt’s, Hodgkin)
Oncogenic virus
Four main morphological virus types
Helical virus
Icosahedron virus
Enveloped virus
Complex virus
Iceberg concept of infection
Base: exposure without attachment (below visual change) or entry; exposure without infection (subclinical)
Viral multiplication without visible change or incomplete viral maturation (below visual change) or infections without clinical illness (asymptomatic infection)
Discernible effect/Apex: inclusion body formation, cell transformation, cell dysfunction
Clinical disease/Apex: moderate severity, mild illness; classic and severe disease (clinical disease)
RBC viral predilection
Parvo B19 (DNA) Pure red cell aplasia
Colorado tick fever virus (RNA)
Monocyte-macrophages predilection
CMV (DNA)
Poliovirus, HIV, measles (RNA)
No cell associated type but bloodstream
Togavirus
Picornavirus
Lymphocyte predilection
EBV, CMV, Hepa V, JC, BK (DNA)
Common cold viral cause
Rhinovirus
Adeno (infant and children)
Corona (adult)
Pharyngitis viral cause
Adenovirus
HSV (infant)
Coxsackie A (children, adult)
Laryngitis or croup viral cause
Tracheobronchitis
Hoarseness “barking” cough
Parainfluenza
Influenza
Bronchiolitis viral cause
Pneumonia
RSV
Subtypes of inlfuenza
A, B, C
2 major influenza antigens
Hemagluttinin (H)
Neuramidase (N)
16 H And 9 N
Influenza A virus subtype H5N1
Avian flu
Influenza A virus subtype H1N1
Swine flu
Most famous segmented virus
Influenza an orthomyxovirus
8 segments that can reassort antigenic drifts and shifts
Influenza A
The two surface antigens of influenza undergo antigenic variation independent of each other
Minor antigenic change is termed
Causes seasonal variation
Antigenic drift
Major antigenic change in HA or NA is called
Results in appearance of a new subtype as in epidemic
Antigenic shift
Antigenic drift is caused by
Accumulation of point mutations in gene
Resulting in amino acid changes in the protein
Sequence changes can alter antigenic sites
Reflects drastic changes in the sequence of a viral surface protein, changes too extreme to be explained by mutation
The segmented genomes of influenza viruses reassort readily in double infected cells
Antigenic shift
All three types of influenza exhibit antigenic drift
Only this type that undergoes antigenic shift because the other types are restricted to humans
Influenza A circulate in animal and bird populations
Account for antigenic shift by genetic reassortment of the glycoprotein genes
Influenza A
Family Parvoviridae
Affects RBCs
Parvo virus
4 Syndromes Associated with Parvo viridae
Erythema infectiosum (Fifth disease)
Transient aplastic crisis (underlying hemolysis)
Pure red cell aplasia (immunodeficiencies)
Hydrops fetalis
Slapped cheek appearance
Lacy appearing rash
Erythema infectiosum
Fifth’s disease
Parvo B19
Causes of hemorrhagic fever
Filovirus
Marburg virus
Ebola virus
Flu like symptoms
Stomach ache
Impaired kidney and liver function
Both internal and external bleeding
Rash, red eyes, hiccup
Ebola virus
Acute febrile illness associated with abrupt onset of headache, myalgia, fever leading to -> rash, shock and bleeding
Ebola virus
Biosafety Level 4 Pathogens due to their high associated mortality rate and aerosol infectivity
Marburg virus
Ebola virus
Biosafety Level 4
Ebola
Smallpox
Biosafety Level 3
H1N1
Yersinia
TB
SARS
Has 5 species named for their original sites of recognition
All 5 are found in Africa (Zaire, Sudan, Cote d’ Ivore, Bundigbugyo) except
Reston
Reston virus was exported from the
Philippines has caused fatal infections in monkeys
Cynomolgus macaque
Most severe Ebola outbreak in history (2014)
Started in Guinea on March 2014
Guinea
Liberia
Sierra Leone
West African Ebola Virus
Successful antiviral used for Ebola and now probable treatment for Corona
Remdesivir
Ebola and Marburg replicate well in all cell types including
Endothelial cells
Macrophages
Parenchymal cells
Earliest involvement in Ebola in macaques are the
Mononuclear pahgocyte system (responsible for initiation of disease process)
Ebola virus on light microscopy
Liver necrosis
Councilman bodies
Intracellular inclusion bodies
Eosinophil inclusion bodies
Apoptotic bodies
Councilman bodies
Conditions where councilman bodies are seen
Ebola virus
Viral hepatitis
Yellow fever
High circulating levels of these are seen in Ebola (Zaire)
Proinflammatory cytokines
Cytokine storm leads to
Lung injury
Renal failure
Heart failure
Pathway complement
Incubation of Ebola
7-10 days
Fever, headache, malaise, myalgia, N/V
Ebola
Ebola virus dx
ELISA - sensitive
PCR
Ebola tx
No specific therapy available
FDA approved EBOLA vaccine
ERVEBO
rVSV ZEBOV
for Zaire Ebola
Tx for Ebola Monoclonal antibody FDA approved reducing viral load in
Regeneron
EBV CA
Burkitt’s
NPC
B cell lymphoma
Hairy leukoplakia in AIDS
Chronic HBV
Primary Hepatocellular CA
Chronic HCV
Primary Hepatocellular CA
HPV CA
Cervical 16,18 Vulvar Vaginal Penile Anogenital
HTLV1 CA
CD4+ T cell leukemia/lymphoma
HHV8 CA
Kaposi sarcoma
HPV 1, 2, 4, 63
Verruca plantaris
Plantar wart
Cervical CA is associated with
HPV 16 18
Paralytic poliomyelitis and ASEPTIC MENINGITIS
feco oral route
Poliovirus
Polio types are classified according to structural differences in the capsid proteins
Serotype 1 (most virulent)
2
3
According to effect
Paralytic polio
Non-paralytic polio
Polio virus predilection with
Anterior Horn Cell
Replicates in the pharynx and GI tract and results in death of motor neurons of
Anterior horn cell of spinal cord
Flu-like symptoms
Sore throat, fever
Non-paralytic polio
Paresthesia
Meningitis
Paralysis (Acute flaccid paralysis-AFP)
Weakness in arms, legs
Paralytic polio
Inoculation of live attenuated polio virus
Orally; Risk of post-polio syndrome
Can infect cells “gut immunity”
Albert Sabin
Inoculation of dead polio virus by injection
Jonas Salk
Aseptic meningitis Herpangina Pleurodynia Myocarditis Pericarditis
Coxsackieviruses
Defined by their pathogenecity in mice
Group A and B
Coxsackievirus mode of transmission
Initial site of infection is the oropharynx or GI tract, then spreads through the bloodstream
Fecal-oral route
Pleurodynia (Bornholm disease)
Myocarditis
Pericarditis
Coxackie B
Herpangina
Hand-foot-and-mouth disease
Coxsackie virus
Enterovirus family
Coxsackie virus A16
Hand foot mouth disease
Double stranded RNA genome composed of 11 segments
Six groups A to F
Rotavirus
Principal cause of human disease
Group A Rotavirus
Only groups A, B and C are known to cause disease in humans
Rotavirus
Attenuated virus Rotarix
Rotateq
Rotavirus
Adverse effect of attenuated virus Rotatrix, Rotateq
Intussuception
First dose of rotavirus should be given after
6 weeks of age
No longer recommended after 2 years and above
Leading cause of morbidity in Filipino children diarrhea
Rota virus
Gold standard for Dx of rotavirus
Viral culture
Sixth disease
Exanthem subitum
Roseola infantum
6 months and 2 years
HHV6
Condylomata acuminatum
HPV
Condyloma lata
Syphilis
Hairy leukoplakia
EBV
SSPE
Measles
Subacute spongiform encephalopathy
Prion
PMLE
JC Virus
SARS
Coronavirus
Bronchiolitis
RSV
Sensorineural deafness
Rubella
Anterior horn cell
Polio
Trigeminal root ganglion
HSV 1
B lymphocytes
EBV
Sacral nerve ganglia
HSV2
DRG
VZV
Fibrolast
CMV
The viral disease that has affected humans throughout recorded history
Earliest physical evidence of smallpox: pustular radh on mummified body of
Paharaoh Ramses V of Egypt
Smallpox
Introduced vaccination with live cowpox in 1798
Edward Jenner
Control of smallpox by deliberate infection with mild forms (ie vaccinia) of the disease
Variolation
In 1967 WHO introduced a worldwide campaign to eradicate smallpox
Case fatality rate decreased fron 25% to 1%
Officially declared eliminated in 1980
Elimination
Smallpox
Reduction to 0 of incidence
Identifed by CDC as first AIDS patient in 1981
Ken Horne
Largest and most complex of virus
Infections are characterized by a rash
Poxvirus
Morphologically distinctive
Exhibit a crisscross pattern
Parapoxvirus
Entire multiplication cycle takes place in the plasm cytoplasm of cells
Poxvirus
More virulent
Variola
Vaccinia
Less virulent
Benign epidermal tumor that occurs only in hunands
Caused by molluscipoxvirus genus
Molluscim contagiosum
Lesions are small, pink, wart-like tumors on the face, arms, back and buttocks
Typical lesion is an umbiillicated lesion
Direct contact and indirect contact (barbers, commo use of towels, swimming pools)
Increasing incidence as an STD in young adults
Molluscum contagiosum
Guarnieri bodies
Variola (smallpox)
Cowdry A virus
HSV/VZV
Cowdry Type B bodies
Polio
Adenovirus
Warthin Finkeldey
Measles
Negri bodies
Rabies
Henderson-Peterson bodies
Molluscum contagiosum
Owl’s eye bodies
CMV