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Virology Flashcards

(41 cards)

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1
Q

Group I

A

dsDNA viruses e.g herpes virus family

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2
Q

Group II

A

ssDNA viruses e.g Parvovirus

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3
Q

Group III

A

dsRNA viruses e.g Rotaviruses

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4
Q

Group IV

A

+ sense RNA viruses e.g HCV, Polio

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5
Q

Group V

A
  • sense RNA viruses e.g influenza, Ebola, measles, rabies
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6
Q

Group VI

A

RNA reverse transcriptase viruses (Retroviruses) e.g HIV

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7
Q

Group VII

A

DNA reverse transcribing viruses (DNA Retrovirus) e.g HBV

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8
Q

DNA virus groups?

A

I, II, VII

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9
Q

Names of all the DNA virus families?

A 
HHAPPPy
Hepadna
Herpes
Adeno
Pox
Parvo
Papova
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10
Q

Which DNA viruses have naked capsids?

A

DNA gets naked for her PAP smear…

Parvovirus
Adenovirus
Papovavirus

Cervical cancer

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11
Q

Which viruses have SEGMENTED genomes?

A

Bunyavirus, Orthomyxovirus, Arenavirus, Reovirus

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12
Q

What is the definition of a Virus?

A

• Obligate intracellular parasite: Depend ENITRELY on the cell they infect for ALL functions i.e replication, to make energy or utilise nutrients

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13
Q

Problems with new emerging viruses?

A

Zoonotic origin (transmitted from animals)

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14
Q

Viroids and Prions

A

• Viroids (no protein) and Prions (no nucleic acid); resistant to radiation damage, heat inactivation, sensitive to urea, SDS and other protein-denaturing chemicals

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15
Q

Capsid

A

• Protein coat that protects virus from the environment (Helical capsid most common (made up of one type of protein)
o Isosahedral capsid Each triangle identically spatial

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16
Q

Nuceloproteins

A

• ALL viruses have NUCLEOPROTEINS (nucleic acid bound to protein)

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17
Q

Assembly of a bacteriophage

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A

STALK (helical) Head (Icosaherdal)

18
Q

Virus replication cycle

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A

• Virus replication cycle: ENTRY (major determinant of tropism), REPLICATION, ASSEMBLY, RELEASE (major determinant of pathogenesis)
o Host cell receptors define: tissue tropism and species tropism i.e is a cell lacks the receptor, it can’t be infected
o Tissue tropism the cells and tissues of a host which supports growth of a particular virus or bacteria
o Pigs can act as an intermediate host (then transfer virus to humans)

19
Q

LOCK AND KEY

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A

interaction of virus will host cell surface receptor is a major determinant of the subsequent events i.e replication/ outcome of infections

20
Q

HIV cell interactions

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A

o CD4 HIV receptor (virus has proteins on its surface which interact with the cell surface)
o Virus tends to have slightly opposite charge to the cell (GAGs) sticks to the cell via static interaction
o 2nd receptor = CCR-5 (lock turns) membrane at the top bought down to meet the membrane at the bottom
o GP41 contains fusion peptide which joins the two membranes together virus inside host cell

21
Q

PENETRATION

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A
  • PENETRATION: pH dependent or pH independent
  • pH dependent: EC virus receptor binding (virus triggers internalisation; instantly transported into a vesicle) viral entry into cytoplasm requires the bursting of the endosome (usually requires acidification by viral proton pumps)
  • pH independent: virus binds to receptor molecule translocated across PM by receptor Virus released into cytoplasm (receptor recycled)
22
Q

Lytic/Chronic release

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A
  • Lytic release destruction of infected cell and its membrane (tend to be naked particles
  • Chronic release Budding borrowing from the cell membrane to create the viruses own membrane (envelope) e.g HIV, Flu
23
Q

Famous 1 step growth curve

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A

Eclipse: Virus inside cell, not detectable, synthesing enzymes, nucleic acid etc
Maturation/Release: MASSIVE increase in growth curves as viruses lyse cells, releasing virion
Plateu: all cells in the culture have been lysed and virus released

24
Q

RNA viruses

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A
  • RNA unstable clover shape protects the end; No poly-A tail (stabalising factor)
  • All proteins that do manufacture assembly are together; all proteins going into the capsid are together; entire virus is one OFR which is cut down to give mature gene products
25
+ Strand RNA virus genomes
* SS, no anti-sense; single START and STOP codon; UTR at start and end; cassette (compartmentalise) their genes like bacteria * Sometimes no poly-a-tail (knot up ends into clover leaf structure) Poly-a-tail prevents the degradation of the message
26
- strand RNA virus genomes
• ANTI-SENSE strand cannot make RNA into protein, therefore the virus has to replicate BEFORE you can get expression of a protein (replication produces sense strand) • Has a polymerase INSIDE the capsid; piece of RNA in the virion • Some SEGMENT their genome more stable/can get more information inside (simple and multi-partite viruses) Fairly simple genetic organisation • ORF..GAP..ORF..GAP • RNA pol, Trimeric envelope, Glycoprotein, Nucleoprotein • Filovirus 1 genome FRAME SHIFTING signals cause it to move around with each frameshift, different protein thrown off PARA and ORTHO myxovirus • Myxo = mucus; ss anti-sense viral genome; causes common cold; effects UPPER RT
27
Influenza
• Ss anti-sense RNA: 7/8 segments (all segments necessary for replication of genome) o These pieces can be moved around and swapped vast majority of influenza particles are defected (lot less viability in particles) o Reassortment of strains can occur in wild ducks, pigs etc NEW flu epidemic o If you infect an organism with two different viruses at the same time, they will MIX at random • Viruses don’t proof read their own polymerase doesn’t check as it goes along ‘genetic drift’ • HN: Neuraminidase found on surface of influenza, enables virus to be released from host cell o Hemagglutinin glycoprotein found on the surface of influenza virus responsible for binding the virus to cells with sialic acid on the membranes
28
Viral Sex
‘’Reassortment’ and swapping of chromosomes massive evolutionary
29
ssRNA replication
* ssRNA needs to form ds RNA replicative intermediate however dsRNA is just plain wrong so ALL RNA viruses will tell you that you are infected as the body recognises this as a foreign agent * 4 basic lifestyle steps total un ivolvement of the nucleus (90-95% of cases)
30
Ds viral replication
* Capsid never fully releases the genome; replication takes place in a partially disassembled shell or ‘skeleton’ never free floating nucleic acids around * Rioviruses very stable on EM can watch what happens during infection
31
Routes of viral entry/Retroviruses
Routes of Viral Entry • PM; endosomes (majority) Retroviruses • Very simple architecturally; very similar to one another; DNA polymerase, reverse transcriptase
32
Why are DNA viruses of interest?
• Why are they of interest? Can cause cancer in humans (apart from adenovirus respiratory disease) o Human adenoviruses infect rodent cells and can turn them cancerous (model system) • HPV16 Papilloma cervical cancer, head and neck cancers • However can have therapeutic uses anti-cancer Herpes simplex to treat solid tumours
33
HOW bad are these viruses?
* 12.7 in 2008 2 mill were infection by virus (approx. 10% = all BC cases) * Causing cancer is not NORMAL part of virus life cycle; DEAD END as new viruses are not made; virus often altered so doesn’t finish life-cycle * Virus-host interactions formed during virus life cycle contribute to carcinogenesis to understand this we need to understand HOW DNA viruses replicate in the host
34
Common persistent infections
* Herpes (e.g Epstein Barr Virus) asymptomatic; stays with us for life; only small % of individuals develop cancer (infection alone not sufficient) other factors involved such as malaria infection (causes Burkitt lymphoma) Nasopharyngeal cancer eating salty fish (nitrosamines) * HPV Hyperproliferative warts (200 genotypes) STI; only small % go on to get cancer; 610,000 cancers caused by HPV usually other factors involved in pathogenesis e.g gene defect, smoking, sun exposure
35
Immune surveillance control
* HIV individuals have MORE cancers caused by these viruses than the general population; HIV patients have a compromised immune system enabling persistence of other infections including cancer causing viruses * These viruses have evolved strategies to hide from our immune system * Organ transplant patients high incidence of cancer caused by genetic viruses
36
Viral DNA replication
* All replicate in the nucleus- except poxviruses; all have different strategies for replication * Requirements: Polymerase + other factors (e.g thymidine kinase) induce the host to express the polymerase * If virus does not encode these factors, has to get them from host if host not making these has to induce host replication factors
37
Where do the replication proteins come from?
• Small DNA viruses do not encode an entire genome replication system encodes proteins that orchestrate the host (polyoma,papilloma,parvo)
38
Viral gene expression
* E + L genes expressed at different times in the life cycle * Viral DNA replication early viral proteins/genes * Once virus has replicated see expression of LATE genes (i.e structural proteins such as capsids) * Replication machinery will only be on and active when our cells are proliferating need to prevent cells dying early proteins stimulate cell growth and stop cell death
39
HPV orchestrates the host cell
• Replicates in squamous epithelia (multi-layered structure) life cycle dependent on differentiation of epithelia • Gains access to basal compartment (parts that are still growing) through cuts/breaks in the epithelia • Virus amplifies its DNA to form new virions in the upper layer of the epithelia virus hits problem as these aren’t proliferating o Proteins E6/E7 upper layers lots of proliferation as lots of new virus is being produced • E7 causes proliferation; in response to this host cell induces apoptosis pathways (problem for virus as it needs to divide) E6 blocks induction of cell death (targets cell regulators which cause cell death) BOTH DEREGULATE TUMOUR SUPPRESSOR PATHWAYS • Targeting TSG lots more host genomic instability therefore increased risk of one of those mutations being an oncogenic mutation proliferation • CERVICAL CANCERS only viral E6 and E7 being expressed.. bad news • Can control E6/E7(viral oncogenes) in lab cancer cells than restore their normal growth
40
Cancer- accumulation of genetic mutations
* Need more than one ‘hit’ ie genetics, diet, chemicals; could be mutations in oncogenes initiates proliferation * Oncogenic viruses: Herpesviridae;Hepadaviridae(HepB vaccine liver cancer; where incidence is high) ;Papillomaviridae;Polyomaviridae,Adenoviridae
41
HPV
* HPV vaccine HPV16L1 protein expressed in insect cells assembled into virus like particles basis for HPV vaccine * Pentamers made up of L1 capsid protein * Very difficult to grow this virus in cell cultures * Took the gene encoding the late protein L1 expressed in bacteria when they looked down the electron microscope saw particles icosahedral capsid just by expressing late protein would assemble spontaneously into a viral capsule form the basis of HPV vaccine * Cervatix, Gardasil * Cervatrix 2 virus like particles * When individuals are vaccinated virus like particles stimulate antibodies can then block infection with infectious HPV 16 and 18. * When the girl is exposed to the actual infectious virus won’t be able to infect * Won’t know true effect for decades

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