Intro to virus Flashcards
all human viruses with helical capsid have
an envelope
Viral envelope
surrounds nucelocapsid, 2 lipid layers with proteins and made from host and virus material. associated with persisitent infections. easy to eliminate with alcohol and detergents.
Hemagglutinin
surface glycoprotein attaches to sialic acid residues of host cell
Neuraminidase
surface spike, aids in release of virus from host cell.
matrix proteins
links envelope and capsid for stabilization, can drive final assembly process and imporant budding location.
viral surface proteins
exposed, made of glycoproteins include VAPS
viral genoms
both linear and circular
DNA envelope viruses
pox, herpes, hepadna
DNA Naked viruses
Polyoma, Papilloma, Adeno, (SS) Parvo
RNA Positive
Naked- Picorna calici, Envelope- Toga, Flavi, Corona
RNA negative
Enveloped Rhabdo, Filo orthomyxo, paramyxo, bunya, arena
Double stranded RNA
Double capsid, Reo
RNA positive via DNA
enveloped Retro.
Biochemical detection for viruses
Enzymatic assays, PCR, NA hybridization
Serological detection for viruses
IF, IP, IB, ELiSA, RIA
Defective Virus
complete virus particle but unable to replicate without helper virus, lacks full complement of genes for complete life cycle
Pseudovirions
contain non-viral DNA, infections but Don’t replicate.
Viriods
subviral, small circular ssRNA genomes, Hep D is the only one for humans and it is enclosed by Hep B.
Prions
proteinaceous and infections, like scrapie,
Virophage
goes after giant virus grows only in a strain of the mimivirus within the infected amoeba sputnik is a circular double stranded DNA
Latent phase
progeny virus accumulates intracellulary, ends when free virus is released.
penetration enveloped vs. non enveleopted
enveloped viruses- endocytosis, fusion with cellular vacuoles or fusion of two membranes
non enveloped, absorptive endocytosis
Protein and nucleic acid synthesis phase
start of eclipse phase, susceptibility is markers and getting into the cell, permissiveness is whether or not it can replicate.
Matrix proteins arrange
alongside the modified cell membrane
nucleocapsid moves
toward the matrix protein area, so it can bud out of the cell.
structural proteins
all proteins in mature virus particle
non-structural proteins
viral proteins in cell but not packaged.
Type 1 Virus
dsDNA virus, Adeno, Herpes, Pox, Polyomaviruses
some can tranform cells
transcribe Immediate Early or Early Mrna
Replication of type 1 virus
IE mRNA translated to IE protein–> IE proteins(regulatory) transcribe EmRNA–>translated to E proteins(regulatory, polymerases)–> replicate parental DNA and LmRNA–> Late mRNA make Late Proteins–> Late proteins make capsids.
Type 2 virus
Single Stranded DNA, very small the circo(sscircularDNA) and parvoviruses(ssLinear DNA).- replication happens in the nucleus and virus is released by cell lysis.
Type 2 replication
ssDNA–> dsDNA by cell enzymes–> mRNA by cell enzymes. –> translated to viral proteins–> make capsids and encapsidate progeny virus.
Type III virus
ds RNA virus must have RNA dependent RNA polyermase in virion. - Reo(rotavirus) and Birna Viruses. replication happens outside of the nucleus inside the capsid to protect it from cells destroying it.
Type III replication
ds RNa is transcribed to viral mRNA by virus associated RNA dependent RNA polymerase, viral mRNA translated to structural and nonstructural proteins. –>mRna are translated resulting in viral proteins assemble to form immature capsid. MRNA is also packaged into the immature capsid then copped within the capsid to form the ds RNAs
Type IV virus
Single stranded Positive sense RNA virus, are infectious, PIcorna, toga, corona, flaviviruses
Type IVa replication
sspositive translted to polyprotein–> transcribe parental positive RNA into negative RNA which is the transcribed to Positive RNA, Structural proteins also translated by polyproteins to make structural proteins–> these make capsids and incorporate progeny RNA
Type IVb replication
SS+RNA makes non structural proteins.–> Parental RNA+ transcribed–>RNA- transcribed into–> RNA+ and capsid incorporates the +RNA
Type V
SS- RNA viruses more diverse, segmentation common, genome is copied by virus specific polymerase- orthomyxo, bunya , filo viruses. Ifluenza
Type v replication
virus associated premade polymerase reads the -RNA –>+RNA serves as intermediate for progeny viral genomes–> mRNA translated–> viral proteins–> assebley of the capsid and incorporation of genomic RNA and viral proteins including virus RNA polymeraase
Type VI Virus
+RNA virus Reverse transcriptase- retroviruses, HIV
Type VI virus replication
2 copies of +RNA: viruas assocatied premade Reverse Transcriptase that generates ds Provrius
Provirus integrates into host genome template for synthesis.
Viral mRNA for non structural and structural proteins, Non structural proteins may be RT and other polymerases, Structural proteins assemble into capsid, Mature virion the capsid incorporates the viral genome and the nucleoproteins including
Type VII ds DNA viruses with ss RNA intermdiate
DNA genomes that use RT to make genomic DNA from an RNA copy HBV,
Type VII replication
Partially DS, DNA complete ds supercoiled DNA is made supercoiled DNA goes to the nucleus for transcription of v0MRNAs and viral pregenomic mRNA–> mRNa translated to structural and nonstructural proteins including polymerase, capsid is made from structural proteins. capsid incorporates the pregenomic mRNA and the viral polymerase. Maturation of the virus–> during this process the pregenomic mRNA–> partially dsDNA–> virus starts to mature.
Epidemic
occur over larger geographical area, introduction of new strain of virus to an immunologically naive population.
Pandemic
worldwide epidemics
virus have cell tropism but cause
more than one disease
viruses encod
virulence factors
virulence factors do these
promote replication and transmission, access to binding to target tisue, escape immune system
Persisting infection
infection without cell death, selection of ideal target (chronic, nonlytic, productive.)
Latent recurring nfection
presence of virus wihtout virus production but with potential for reactivation
susceptible host
has proper receptors
permissive host
has proper biosynthetic machinery
GI tract infections have more significant effect on
infants (dehydration,) undernourished people.
Macule
flat colored spots
papules
slightly raised areas from immune response
Nodules
larger raised areas of the skin
vesicular lesions
blisters likely to contain virus.
hemorrhagic fevers
infect endothelial cell lining of the vasculature possibly compromising the structure of the blood vessel.
HHV 1 and 2 virus
can initally infect and replicate mucoepithelial cells, are lytic most cells: cowdry type A inclusion bodies synctia- persistent (lymphocytes and macrophages) latent infections (neurons)
–virus blocks effects of interferon, prevents T cell recognition of infected cells and escapes antibody neturialization.
–recurrence occurs.
HHV- 5 CMV
chorioretinitis is associated with CM in newborns. most prevalent viral cause of congenital disease
Cytopathic Effects
Rounding, inclusion bodies, cell lysis, necrosis, apoptosis, scyncythia formation, transformation.
No human cancer arises
as the acute consequence of infection jusually latency periods between primary infection and cancer development.
no synthesis of the infectious gents occurs in
cancer cells.
most cancer causing viruses are
common in the population.
papilloma transforms proteins
E6, E7
Polyoma transforms proteins
Large T and Small T antigen
Adenovirus transforms
E1A and E1B
BK virus and SV-40 virus transforms
Large T
EBV HHV4
EM observation characterisitic herpes, causally associated with AfBL hodkindisease and NPC, also been asosciated with B-cell lymphonmas in patients.
EBV proteins encodes
LMP proteins, EBNA proteins vIL 10
HHV-8 Kaposi’s sarcoma
tumor of the blood vessel, rare in people not infected with HIV
Merkel cell polyomavirus
highly aggressive neuroendogrine carcinoma
Mutated genes in HBC
HBx and PreS mutants
Mutated genes in HBV
Core NS2 NSSB
RNA tumor viruses
-some retroviruses have oncogenes in addition to regular genes some –can integate particular sites in host cells(oncogenes is by promoter sequence)
- retroviruses particularly on original
-acute leukemia or sarcoma(fast) and leukemia(slow)
Fast: oncogene- direct effect provision of growth enhancing proteins
slow: transactivation- indirect effect transactivation protein(tax)!or long terminal repeat promoter sequences that enhance expression of cellular growth genes.
HTLV -1
retrovirus known to cause human cancer. cause cancer after a long latency period, more indirect than the encoding viruses. causes adult acute t cell lymphocytic leukemia (ATLL) and HTLV associated myelopathy
HTLV uses gene
TAX
Non Hodgkin’s lymphoma:
most common among those w/ inherited immune deficiency, autoimmune disease or HIV. can increase risk by HTLV-1 hep C and EBV
Example of subunit vaccines
HepB, quadrivalent HPV 6/11/16/18 and L1 VLP vaccin.
HPV vaccine
Recombinant L1 proteins that self assemble into VLP’s administered before the onset of sexual activity, 100% protection from infection with vaccine HPV types ptoential to prevent 70% cervical cancers and 90% genital wards.
Antivirals
interfere with virus specific function, interfere with cellular function, are water soluble and taken up by cells not stable. toxic carcinogenic allergenic mutagenic teratogenic used more for prophylaxis
action of antiviruals
block attachment, penetration, uncoating.
antivirals can also inhibt
function of viral DNA polymerase
Acyclovir can be used for
treatment of HHV I and HHV II infections
Acyclovir mechanism
guanosine analog must undergo thymidine kinase mediated phosphorylation acyclovir trphosphate blocks DNa synthesis by chain termination.
Nevirapine
non nuleoside polymerase inhibitr bind to various enzyme sites.
antiviral protease inihibitor
saquinavir block cleavage of polyproteins, hIB dependent on proteolytic enzyme for full infectivity. drug resistant strains protease mutations.
Imiquimod
toll like receptor ligand stimulates innate responses to attck the virus infection. HPV
