viral basics Flashcards
type of recombination with viruses with a segmented genome (only RNA viruses)
2 strains of same virus infect same cell → exchange intact genetic SEGMENTS→ limited epidemic, world-wide pandemic
i.e., RNA influenza
reassortment
2 viruses infect same cell → exchange GENES between 2 chromosomes in regions of genetic homology → viral progeny are not like parent viruses
i.e., DNA viruses or RNA viruses with DNA phase (retroviruses)
recombination
2 viruses infect same cell - one virus has a mutation → makes non-functional protein but nonmutated virus can make a functional protein that can allow the mutated virus to replicate itself
mutated virus can only replicate through complementation: infect host cell or another virus can provide functional protein
complementation
2 viruses infect same cell → progeny virions receive surface proteins from 1 or both parent viruses → alters tissue type the virus can infect but the genetic material inside only came from 1 of the parents (no change to genetic material) → progeny will have the coat coded by genetic material
phenotypic mixing
number of copies of RNA or DNA present in virion
all DNA and RNA viruses are haploid (only 1 copy) EXCEPT retrovirus (2copies of ssRNA)
virus ploidy
contain live virus but weakened → subclinical infection to allow for humoral + ROBUST cell-mediated immunity
long-lasting immune response
rare: attenuated vaccine reverted to wild-type
live attenuated vaccine
from whole, killed virus
humoral + cell-mediated (not as robust)
may need BOOSTER
killed virus vaccines
use specific viral antigens to stimulate immune response
subunit viral vaccines
enveloped DNA virus
latent infection in host cell
reactivation disease after recovery from acute infection
8 human herpesviruses (HHV)
lab test to detect HSV-1 or HSV-2 or VZV
Tzanck smear: multinucleated giant cells = + test (one of these viruses)
low specificity and sensitivity
scrape base of open vesicle
type A cowdry bodies or type 1 cowdry inclusions
intranuclear eosinophilic inclusions seen in
HSV-1 or HSV-2 or VZV
symptoms of mono (fever, sore throat, posterior cervical LAD - painful, exudative pharyngitis) but
- heterophile test (monospot)
no EBV antibodies
CMV infection (most common) acute HIV acute toxoplasmosis viral hepatitis strep throat
EBV associated malignancies: EBV is latent inside body and contributes to cancer
Hodgkin lymphoma: 50% cases burkitt lymphoma nasopharyngeal carcinoma diffuse large cell lymphoma oral hairy leukoplakia lymphoproliferative disorders
owl’s eye nuclear inclusions
CMV
causes roseola (sixth disease/exanthema subitum vs parvovirus B19 = fifth disease) in children almost all infected by 2 yo
HHV-6
3-5 days of high fever (>102 F) → then, body-wide maculopapular rash
latent infection - no known concerns
complication: febrile seizures
roseola from HHV-6
roseola-like infection (but later in life)
latent infection - no known concerns
all infected by 5 yo
HHV-7
5% total U.S. population infected
MSM - prevalence is much higher
infects spindle cells coming from vascular and lymphatic endothelial tissue (inner lining of blood vessels and lymphatic vessels)
highly vascular tumors:
purple lesion on skin +/- organ systems (lung (hemoptysis): nodule on chest CT)
HHV-8 (kaposi sarcoma-associated herpesvirus)
treatment of HHV-8 (kaposi sarcoma-associated herpesvirus)
HAART (HIV retroviral therapy)
topical agents: alitretinoin
intralesional: vinblastine
liposomal anthracyclines: daunorubicin, doxorubicin
types of HHV-8 (kaposi sarcoma-associated herpesvirus)
classic: slow-growing tumor without much potential for mets
epidemic: found in HIV/AIDs patients
immunocompromised: transplant patients
latent herpes virus locations
HSV-1: trigeminal ganglia HSV-2: sacral ganglia VZV: dorsal root or trigeminal ganglia CMV: mononuclear cells EBV: B cells
downey cells: foamy cytoplasm
T cells that respond to EBV infected B cells
REASSORTMENT of viral genome
1 pig infected with 2 influenza A viruses: 2 virus genomes can exchange genetic material
between human and pig viruses → now pig genetic material in human virus →infect humans → no preexisting immunity for pig virus in humans → PANDEMIC
genetic shift
“oh SHIFT***” = bigger deal
genes become mutated or rearranged
small changes in influenza virus every year (reason for seasonal VACCINE) → immune system can better handle → seasonal EPIDEMICS
genetic drift
trivalent flu vaccine components
2 influenza A
1 influenza B
chosen based on pattern of flu infections over last year
quadrivalent flu vaccine components
2 influenza A
2 influenza B
intranasal flu vaccine
live attenuated virus
intranasal
healthy, non-pregnant adults: 2-49 yo
injectable flu vaccine
killed virus
effectiveness of flu vaccine depends on
typical effectiveness at preventing infection: 60-80%
also ↓ disease severity
effectiveness depends on:
age of person
immune system
when received: takes 2 weeks for Abs to develop
how well matched to strains
age recommended to get flu shot
equal to or greater than 6 mo
winter infections
influenza: flu
rotavirus: diarrhea in kid
RSV: bronchiolitis in kid
summer infections
1) enterovirus: poliovirus echovirus coxsackievirus 2) arbovirus: west nile virus
hepatitis C treatment
ribavarin
INFα
illnesses spread by rodent urine
RNA viruses: hantaviurs lassa virus LCM virus bacteria: leptospirosis
