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INF > CELL BIOLOGY OF VIRUSES > Flashcards

CELL BIOLOGY OF VIRUSES Flashcards

1
Q

MEANING OF THE WORD VIRUS?

A

LATIN FOR POISON

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2
Q

VIRUSES WERE FIRST DISCOVERED BECAUSE OF THEIR ROLE IN?

A

ROLE IN PRODUCING DISEASE IN AGRICULTURALLY IMPORTANT PLANTS AND ANIMALS

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3
Q

WORK ON WHICH DISEASES FIRST LEAD TO THE WORD VIRUS TO MEAN ANY INFECTIOUS AGENT SO SMALL THAT IT COULD BE NEITHER OBSERVED BY LIGHT MICROSCOPY NOR REMOVED FROM A SOLUTION BY FILTRATION THROUGH THE SMALLEST PORES THAT HUMANS COULD MANUFACTURE?

A

TOBACCO MOSAIC DISEASE

FOOT-AND-MOUTH DISEASE

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4
Q

ONE OF THE FIRST DEFINITIONS OF VIRUSES?

A

ANY INFECTIOUS AGENT SO SMALL THAT IT COULD BE NEITHER OBSERVED BY LIGHT MICROSCOPY NOR REMOVED FROM A SOLUTION BY FILTRATION THROUGH THE SMALLEST PORES THAT HUMANS COULD MANUFACTURE

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5
Q

WHAT IS A CHAMBERLAND FILTER AND HOW DOES IT RELATE TO VIRUSES?

A
  • NAMED AFTER CHARLES CHAMBERLAND (1851-1908)
  • C.C. DISCOVERED THAT WARM PORCELAIN CAN RETAIN FINE PARTICLES IN SOLUTION AND, ALONG WITH LOUIS PASTEUR, SHOWED THAT BACTERIA CAN BE FILTERED OUT OF A SOLUTION USING A PORCELAIN FILTER IN A GLASS TUBE
  • VIRUSES WERE FIRST UNDERSTOOD AS MICROBES SO TINY THAT THEY COULD PASS THROUGH A CHAMBERLAND FILTER
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6
Q

USUAL SIZE OF VIRUSES?

A

20-100 nm IN DIAMETER

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7
Q

MICROSCOPY FOR OBSERVING VIRUSES?

A
  • MOST VIRUSES ARE TOO SMALL TO BE SEEN USING LIGHT MICROSCOPY
  • LIGHT MICROSCOPY USEFUL FOR STUDYING VIRAL EFFECTS ON CELLS
  • VIRUSES ARE USUALLY VISUALISED USING ELECTRON MICROSCOPY OR ATOMIC FORCE MICROSCOPY
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8
Q

IS HERPESVIRUS A SMALL OR A LARGE VIRUS?

A

LARGE (200nm)

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9
Q

WHICH OF THESE CANNOT BE USED FOR OBSERVING VIRUSES - LIGHT MICROSCOPY, ATOM FORCE MICROSCOPY, ELECTRON MICROSCOPY

A

LIGHT M.

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10
Q

NAME OF A LARGE VIRUS COVERED BY SURFACE FIBERS, WITH A DISTINCTIVE STAR-SHAPED DEPRESSION?

A

MIMIVIRUS

very big, has a huge genome, initially mistaken for bacteria

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11
Q

WHAT ARE CYTOPATHIC EFFECTS AND WHAT DO THEY DEPEND ON?

A

Cytopathic effect or cytopathogenic effect (abbreviated CPE) refers to structural changes in host cells that are caused by viral invasion.
DEPENDS ON THE SPECIFIC HOST CELL AND THE VIRUS

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12
Q

WHAT ARE VIRUS-INDUCED SYNCITIA (SYNCYTIA)?

A

LARGE, MULTINUCLEATE CELLS
Viral protein mediates fusion of an infected cell with neighboring cells leading to the formation of multi-nucleate enlarged cells called syncytia.

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13
Q

EXAMPLES OF CYTOPATHIC EFFECTS DUE TO VIRAL INFECTIONS?

A
  • MANY VIRUSES CAUSE INFECTED CELLS TO ROUND UP AND DETACH FROM TISSUE FLASK AS THEY DIE (E.G. PANCREATIC NECROSIS VIRUS)
  • SOME VIRUSES CAUSE CELLS TO FORM SYNCITIA (LARGE, MULTINUCLEATE CELLS)
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14
Q

4 TRAITS THAT DEFINE VIRUSES?

A

1) VIRUSES ARE OBLIGATE INTRACELLULAR PARASITES THAT HAVE AN INFECTIOUS EXTRACELLULAR STAGE, CALLED VIRION
2) ALL VIRUSES ENCODE AT LEAST ONE CAPSOMERE PROTEIN, CAPSOMERES COVER AND PROTECT THE NUCLEIC ACID IN A VIRION, AN ALL VIRUSES CARRY GENETIC INSTRUCTIONS FOR SYNTHESIZING AT LEAST ONE CAPSOMERE
3) ALL VIRUSES REPLICATE, NOT BY GROWING LARGER AND DIVIDING AS DO CELLS, BUT BY ASSEMBLY (CELLS INFECTED BY VIRUSES SYNTHESIZE THE COMPONENT PARTS OF THE VIRION, AND THEN HE PARTS, ONCE SYNTHESIZED, SPONTANEOUSLY ASSEMBLE INTO NEW VIRIONS WITHOUT FURTHER INPUT OF ENERGY
4) ALL VIRUSES HAVE THE CAPACITY TO EVOLVE (BECAUSE THE MINIMUM COMPOSITION OF VIRUSES IS NUCLEIC ACIDS AND CAPSOMERES, VIRAL POPULATIONS CAN CHANGE THROUGH TYPICAL EVOLUTIONARY PROCESSES THAT ALTER THOSE NUCLEIC ACIDS IN A HERITABLE WAY

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15
Q

WHAT IS THE MINIMUM COMPOSITION OF VIRIONS?

A

NUCLEI ACIDS AND CAPSOMERES

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16
Q

HOW TO VIRAL POPULATIONS USUALLY EVOLVE?

A

THROUGH TYPICAL EVOLUTIONARY PROCESSES THAT ALTER THEIR NUCLEIC ACIDS IN A HERITABLE WAY

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17
Q

NAME AND EXPLANATION OF THE PROCESS VIRUSES USE TO REPLICATE?

A

ASSEMBLY
CELLS INFECTED BY VIRUSES SYNTHESIZE THE COMPONENT PARTS OF THE VIRION, AND THEN THE PARTS, ONCE SYNTHESIZED, SPONTANEOUSLY ASSEMBLE INTO NEW VIRIONS WITHOUT FURTHER INPUT OF ENERGY

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18
Q

WHICH TYPE OF PROTEIN IS ENCODED BY EVERY VIRUS?

A

AT LEAST ONE CAPSOMERE PROTEIN IS ENCODED BY EVERY VIRUS

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19
Q

WHAT ARE CAPSOMERES?

A

STRUCTURES THAT COVER AND PROTECT THE NUCLEIC ACIDS (GENETIC MATERIAL) IN VIRUSES

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20
Q

WHAT IS THE EXTRACELLULAR INFECTIOUS STAGE OF VIRUSES CALLED?

A

VIRION

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21
Q

WHAT IS CAPSID?

A

PROTEIN COAT OF CAPSOMERES THAT SURROUND THE NUCLEIC ACIDS IN VIRUSES

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22
Q

EXPLAIN THE TERM NUCLEOCAPSID?

A

IN SOME VIRUSES, THE NUCLEIC ACID GENOME AND THE PROTECTIVE STRUCTURES AROUND IT, CAPSOMERES, ARE SO INTIMATELY ASSOCIATED THAT THEIR JOINT STRUCTURE IS CALLED NUCLEOCAPSID (e.g. SARS CoV 2)

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23
Q

DIFFERENCE BETWEEN ENVELOPED AND NAKED VIRIONS?

A

ENVELOPED VIRIONS HAVE A LIPID BILAYER, WHEREAS NAKED VIRIONS DO NOT

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24
Q

DESCRIBE THE SPHERICAL CAPSIDS IN VIRUSES?

A
  • ICOSAHEDRONS (POLYHEDRONS WITH 20 FACES) CONSTRUCTED FROM REPEATED UNITS, APPROXIMATING A SPHERE
  • SOMEWHAT RIGID, COMPARED TO E.G. HELICAL CAPSIDS THAT CAN BE RIGID OR FLEXIBLE
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25
Q

WHAT IS THE BALTIMORE CLASSIFICATION SCHEME?

A
  • FIRST DEFINED IN 1971
  • THE SCHEME DERIVED FROM THE MECHANISM BY WHICH THE VIRAL GENOME IS RELATED TO mRNA (CLASSES BASED ON THE WAY THE VIRUSES USE AND PRODUCE RNA)
  • CLASSIFICATION SYSTEM THAT PLACES VIRUSES INTO ONE OF SEVEN GROUPS DEPENDING ON A COMBINATION OF THEIR NUCLEIC ACID (DNA OR RNA), STRANDEDNESS (SINGLE OR DOUBLE STRANDED), SENSE, AND METHOD OF REPLICATION
  • GROUPS DESIGNATED BY ROMAN NUMERALS
  • E.G. GROUP I ARE DS DNA VIRUSES, GROUP II SS DNA VIRUSES, III:DS RNA…
    (it does NOT reflect evolutionary relatedness of different groups of viruses)
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26
Q

WHAT ARE THE MOST ABUNDANT EVOLVING ENTITIES?

A

VIRUSES

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27
Q

NUMBER OF VIRUSES COMPARED TO THE NUMBER OF BACTERIAL AND ARCHEAL CELLS ON EARTH?

A

10x MORE VIRUSES

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28
Q

ALL LIVING MICROBES SHARE A TRAIT OF HAVING ENERGISED MEMBRANES; EXPLAIN THIS TRAIT + ARE VIRUSES ALIVE BASED ON THIS DEFINITION?

A

One trait shared by all living microbes, is that they have an energized membrane in which the concentration of ions is different in the two compartments separated by that membrane. For a microbial cell, dissipation of the ion gradients is the definitive sign that the cell is no longer alive.
By this definition there are no living viruses because even though some viruses have a lipid bilayer, called a viral envelope, the viral envelope is not energized!!!

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29
Q

WHAT IS THE VIRAL LIPID BILAYER THAT SOME VIRUSES HAVE CALLED?

A

VIRAL ENVELOPE

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30
Q

WHAT ARE SPIKE PROTEINS (PEPLOMERS)?

A

In virology, a spike protein or peplomer protein is a protein that forms a large structure known as a spike or peplomer projecting from the surface of an enveloped virus. The proteins are usually glycoproteins that form dimers or trimers. Often the term “spike protein” refers specifically to the coronavirus spike protein, one of the four major structural proteins common to all coronaviruses, which gives rise to the distinctive appearance of these viruses in electron micrographs (projections from a spherical capsid). These proteins typically have a role in viral entry.

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31
Q

% OF THE HUMAN GENOME THAT IS MADE UP OF 100,00 PARTIAL SEGMENTS OF HUMAN ENDOGENOUS RETROVIRUSES (and their role?)

A

8%

(Endogenous retroviruses are associated with major evolutionary events, including the origin of Homo sapiens; retroviral infections are likely causing evolutionary change today)

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32
Q

HUMAN ENDOGENOUS RETROVIRUSES IN THE GENOME MAY BE ASSOCIATED WITH THE FORMATION OF WHICH HUMAN ORGAN?

A

PLACENTA

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33
Q

WHAT IS RAPID EVOLUTIONARY RADIATION?

A

AN EVOLUTIONARY PROCESS IN WHICH MANY SPECIES SEEM TO APPEAR FROM A COMMON ANCESTOR IN A SHORT PERIOD OF TIME ON AN EVOLUTIONARY SCALE

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34
Q

HOW ARE HUMAN ENDOGENOUS RETROVIRUSES IN THE HUMAN GENOME ASSOCIATED WITH PLACENTA DEVELOPMENT?

A
  • THE DEVELOPMENTAL PROGRAM TO BUILD MAMMALIAN PLACENTA DEPENDS ON SYNCYTIN, WHICH IS THE ENVELOPE GENE OF HUMAN ENDOGENOUS DEFECTIVE RETROVIRUS, HERV-W
  • PLACENTAL SYNCYTIOTROPHOBLASTS (MULTINUCLEATED CELLS THAT ORIGINATE FROM FETAL TROPHOBLASTS) ARE MAJOR SITES OF SYNCYTIN EXPRESSION
  • EXPRESSION OF RECOMBINANT SYNCYTIA IN A WIDE VARIETY OF CELL TYPES INDUCES FORMATION OF A GIANT SYNCYTIA
    (INFECTION BY A RETROVIRUS MADE THE EMERGENCE OF PLACENTAL MAMMALS POSSIBLE BY PROVIDING A VIRAL PROTEIN THAT ENABLS FORMATION OF THE PLACENTA)
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35
Q

VIRIONS?

A

THE EXTRACELLULAR INFECTIOUS PARTICLES THAT CARRY VIRAL NUCLEIC ACIDS FROM ONE HOST CELL TO ANOTHER
- ALL ARE MADE UP OF, AT A MINIMUM, PROTEIN CAPSOMERES ENCLOSING NUCLEIC ACIDS

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36
Q

TYPES OF VIRIONS BASED ON SHAPE AND ENCLOSURE?

A

VIRUSES CAN BE ICOSAHEDRAL OR HELICAL = NAKED OR ENVELOPED

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37
Q

DESCRIBE VIRAL GENOME DIVERSITY?

A
  • CAN BE COMPOSED OF DNA OR RNA
  • CAN BE ARRANGED AS LINEAR OR CIRCULAR MOLECULES THAT ARE EITHER DOUBLE OR SINGLE STRANDED AND EITHER SEGMENTED OR NON SEGMENTED
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38
Q

STAGES OF THE VIRAL REPLICTION CYCLE?

A

1) ATTACHMENT (THE VIRION ATTACHES TO THE HOST CELL)
2) PENETRATION AND UNCOATING (THE VIRION’S GENOME ENTERS THE HOST CELL: IN DOING SO, THE VIRUS AS A DISCRETE VIRION CEASES TO EXIST, BEGINNING THE ECLIPSE PERIOD) —> THE GENOME SOMETIMES ENTERS WITH THE CAPSID OR PIECES OF THE CAPSI
3) SYNTHESIS OF EARLY PROTEINS (THE PROTEINS EXPRESSED EARLY IN AN INFECTION OFTEN GIVE ONE OF 3 FUNCTIONS: SHUT DOWN HOST PROTEIN SYNTHESIS, REGULATE XPRESSION OF VIRAL GENES, SYNTHESISE VIRAL NUCLEIC ACIDS)
4) SYNTHESIS OF NEW VIRL GENOMES AND LATE PROTEINS (LATE PROTEINS ARE THOSE EXPRESSED AFTER GENOME REPLICATION HAS BEGUN, USUALLY STRUCTURAL PROTEINS, MEANING THEY WILL BECOME COMPONENTS OF THE PROGENY VIRIONS)
- ————– STAGES 3 AND 4 OVERLAP IN SOME VIRUSES, ESP THOSE WITH SMALL GENOMES
5) ASSEMBLY (COMPONENT PART OF THE VIRION ASSEMBLE INTO COMPLETED VIRIONS)
6) RELEASE (THE RELEASE OF THE NEWLY ASSEMBLED VIRUSES, THE LAT STEP, CAN BE SUDDEN OR GRADUAL, ULTIMATELY KILLING CELLS)

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39
Q

WHAT IS THE VIRAL ECLIPSE PERIOD?

A

the time between infection by (or induction of) a bacteriophage, or other virus, and the appearance of mature virus within the cell; an interval of time during which viral infectivity cannot be recovered
- begins after virion’s genome enters a host cell (AND THE VIRUS AS A DISCRETE VIRION CEASES TO EXIST)

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40
Q

WHT ARE EARLY PROTEINS IN VIRAL REPLICATION?

A
  • PROTEINS EXPRESSED EARLY IN AN INFECTION
    USUALLY HAVE ONE OF 3 FUNCTIONS:
  • SHUT DOWN THE SYNTHESIS OF HOST PROTEINS
  • REGULATE EXPRESSION OF VIRAL GENES
  • SYNTHETISE VIRAL NUCLEIC ACIDS
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41
Q

WHAT ARE LATE PROTEINS IN VIRAL REPICTION?

A
  • PROTEINS EXPRESSED AFTER THE GENOME REPLICATION HAS BEGUN

- USUALLY STRUCTURAL PROTEINS, HICH WILL ACT AS COMPONENTS OF FUTURE VIRIONS

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42
Q

EXAMPLES OF VIRUSES WITH SUDDEN VS GRADUAL RELEASE OF NEWLY SYNTHESISED VIRIONS AFTER INFECTED THE HOST?

A
  • BACTERIOPHAGES RELEASE IS SUDDEN BECAUSE LYSIS OF THEIR HOST CELLS MUST OCCUR IN ORDER FOR VIRUS TO ESCAPE
  • SHEDDING OF VIRUSES FROM ANIMAL CELLS CAN BE GRADUAL AND MAY NOT LYSE THE HOST CELLS
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43
Q

DESCRIBE THE ONE-STEP GROWTH CURVE OF VIRAL GROWTH

A
  • AFTER A SINGLE VIRUS IS ADDED TO ITS HOST CELL, EXTRACELLULAR VIRUSES BECOME UNDETECTABLE DURING THE ECLIPSE PERIOD
  • THEN, IN AN ABRUPT CHANGE, THE NUMBER OF EXTRACELLULAR VIRUSES INCREASES EXPONENTILLY
  • EVENTULLY THE NUMBER OF VIRUSES LEVELS OFF, AND THERE IS NO FURTHER INCREASE IN THE POPULATION SIZE
    GRAPH DESCRIPTION:
  • NUMBER OF VIRUSES = 0 (Y=0), THE POINT JUST MOVING ALONG THE X AXIS (TIME)
  • AFTER A CERTAIN X HAS BEEN REACHED THERE IS A SHARP EXPONENTIAL RISE ALONG THE Y AXIS, WHICH SOON REACHES A PEAK AND REMAINS CONSTANT
    (once virion is taken up by the cell no change is detected for awhile and then there is a sudden sharp rise in the number of viruses after replication in the cell)
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44
Q

DESCRIBE THE ORDER OF SYNTHESI OF VIRAL COMPONENTS DURING AN INFECTION?

A

FROM 1ST O LAST TO START FORMING:VIRAL MRNA, VIRAL PROTEINS, VIRAL GENOMES, INTRACELLULAR VIRUSES, EXTRACELLULAR VIRUSES (THEY STOP BEING PRODUCED IN THE SAME ORDER, AS THEY ARE REQUIREMENTS FOR ONE ANOTHER)

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45
Q

INFLUENZA VIRUS OVERVIEW

A

Influenza type A viruses are RNA viruses categorized into subtypes based on the type of two proteins on the surface of the viral envelope:

H = hemagglutinin, a protein that causes red blood cells to agglutinate.
N = neuraminidase, an enzyme that cleaves the glycosidic bonds of the monosaccharide sialic acid (previously called neuraminic acid).
The hemagglutinin is central to the virus’s recognizing and binding to target cells, and also to its then infecting the cell with its RNA. The neuraminidase, on the other hand, is critical for the subsequent release of the daughter virus particles created within the infected cell so they can spread to other cells.

Different influenza viruses encode for different hemagglutinin and neuraminidase proteins. For example, the H5N1 virus designates an influenza A subtype that has a type 5 hemagglutinin (H) protein and a type 1 neuraminidase (N) protein. There are 18 known types of hemagglutinin and 11 known types of neuraminidase, so, in theory, 198 different combinations of these proteins are possible.

Variants are sometimes named according to the species (host) in which the strain is endemic or to which it is adapted. The main variants named using this convention are:

Bird flu
Human flu
Swine influenza
Equine influenza
Canine influenza
Bat influenza
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46
Q

INFLUENZA A VIRUS BASED ON ITS DNS?

A

negative-sense, single-stranded, segmented RNA viruses

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47
Q

positive vs negative stranded viruses?

A

Positive-stranded RNA is just like mRNA can be read natively by the host’s translational machinery to make proteins
Negative-stranded RNA is complementary to mRNA AND must be transcribed into a positive strand by the virus’s own RNA-dependent RNA polymerase (this enzyme is carried in the capsid of all negative-stranded RNA viruses)
Most DNA viruses have both a positive and negative strand

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48
Q

WHAT DOES THE TERM ‘POLYCISTRONIC’ REFER TO WHEN DESCRIBING MRNA? IS IT TYPICAL OF PROKARYOTES OR EUKARYOTES?

A

The term “polycistronic” describes the situation in which two (bicistronic/dicistronic), three (tricistronic), or more separate proteins are encoded on a single molecule of messenger RNA (mRNA): thy have separate start and stop codons. In prokaryotes, polycistronic expression is common. (EUKARYOTIC MRNA ENCODES JUST ONE PROTEIN WITH A WINGLE START AND STOP CODON)

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49
Q

WHAT ARE VIRUS REPLICATION COMPLEXES (VRC)?

A
  • ASSEMBLY FACTORIES IN EUKARYOTIC VIRUSES

- ASOCIATED WITH VARIOUS MEMBRANES, SUCH AS ER OR GOLGI BODY, IN ADDITION TO THE PLASMA MEMBRANE

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50
Q

HOW DOES THE HERPESVIRUS EXIT THE NUCLEUS?

A

BY BUDDING (Budding enables viruses to exit the host cell and is mostly used by enveloped viruses which must acquire a host-derived membrane enriched in viral proteins to form their external envelope. Viruses can bud at every stage in the ER-Golgi-cell membrane pathway.)

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51
Q

PROCESS BY WHICH BACTERIOPHAGES PERFORM VIRAL RELEASE IN HOST CELLS IS CALLED?

A

OSMOTIC LYSIS (BACTERIOPHAGES ENCODE CELL-WALL DEGRADING ENZYMES SO THAT THE PHAGES CAN ESCAPE LEADING TO THE OSMOTIC LYSIS)

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52
Q

HOW ARE PLANT VIRUSES CARRIED FROM ONE PLANT TO ANOTHER?

A

BY BITING ARTHROPODS, WHOSE MOUTH PARTS BREAK THROUGH THE PLANT CELL WALL

53
Q

WHICH CELLS ARE THE HOSTS FOR THE HIV VIRUS?

A

CD4+ LYMPHOCYTES (NUMBER OF HIV VIRIONS IN BLOOD IS CONVERSLY ASSOCITED WITH THE CONCENTRATION OF THE CD4+ LYMHOCYTES)

54
Q

VIRUS FORMALLY KNOWN AS HUMAN HERPESVIRUS 1 IS NOW CALLED?

A

THE HERPES SIMPLEX VIRUS

55
Q

EXAMPLE OF A LATENT INFECTION IN HUMANS? = DESCRIBE THE FUNCTIONING

A
  • HERPESVIRUSES ARE A CLASIC EXAMPLE
  • THE VIRUS AFFECTS BOTH EPITHELIAL TISSUES AND TERMINLLY DIFFERENTIATED NEURONS
  • THE EPITHELIAL INFECTIONS TYPICALLY CUSE GENITAL OR ORAL SORES CHARACTERISTIC OF A HERPES INFECTION
  • HOWEVER, THE VIRUS CAN ALSO PRODUCE A QUIESCENT INFECION IN NEURONS WITHOUT PRODUCING VIRIONS FOR THE LIFETIME OF AN INFECTED PERSON
  • LATENTLY AFECTED NEURONS APPEAR NORMAL IN TISSUE CULTURE
  • SPORADICALLY OR IN REPONSE TO STRESS, THE LATENT VIRUS REACTIVATES AND THE INFECTED NEURON BEGINS TO PRODUCE INFECTIOUS PARTICLES
  • THESE PARTICLES ARE RELEASED AND SUBSEQUENTLY INFECT EPITHELIAL CELLS ENERVATED BY THAT PARTICULAR NERVE, WHICH ULTIMATELY CAUSES MORE HERPES LESIONS WITH THE POTENTIAL TO SPREAD THE VIRIONS TO OTHER PEOPLE
56
Q

WHICH EXPERIMENT WAS ESSENTIAL FOR DISCOVERING THE PHASES OF THE VIRUS REPLICATION CYCLE?

A

THE ONE-STEP GROWTH EXPERIMENT (allows the calculation of both the duration of the different phases and the yield of the viral cycle (also known as burst size, that is, the number of virions produced by each infected cell)

57
Q

AN ECLIPSE PERIOD IS UNIQUE TO?

A

VIRUSES

58
Q

THE STAGES 3 AND 4 OF THE VIRUS REPLICATION CYCLE (I.E. EXPRESSION OF EARLY VIRL PROTEINS AND GENOME REPLICATION) USULLY OVERLAP IN WHICH VIRUSES?

A

THOSE WHICH HAVE A SMALL GENOME SIZE

59
Q

EXAMPLE VIRUS FOR A LYTIC VIRAL INFECION IN HUMANS?

A

THE INFLUENZA VIRUS

60
Q

THE INFLUENZA VIRUS EXITS HOST CELLS THROUGH…

A

BUDDING

61
Q

DIFFERENTIATION OF LONG TERM INFECTIONS?

A

LYTIC INFECTIONS: VIRIONS CONSTANTLY PRODUCED (INFLUENZA)
LATENT INFECTIONS: VIRIONS NOT PRODUCED AT ALL (HERPES)
HIV CAUSES BOTH CHRONIC LYTIC AND LATENT INFECTIONS!!!!

62
Q

WHERE IN A HOST CELL CAN EUKARYOTIC VIRUSES SYNTHESISE MRNA AND NEW GENOMES?

A

THE CAN DO IT BOTH IN THE NUCLEUS OR THE CYTOPLASM

  • PARTICULAR INTERACTIONS BETWEEN CERTAIN SUBCELLULAR COMPONENTSOF HOST CELLS AND THE VIRUS ARE RESPONSIBLE FOR ADVANCING THE VIRUS THROUGH THE REPLICATION CYCLE
  • VIRUS REPLICATION COMPARTMENTS ARE TYPICALLY FOUND IN CLOSE ASSOCIATION WITH CELLULAR MEMBRANES, WHICH ARE TYPICALLY MODIFIED TO CONTAIN VIRAL PROTEINS
63
Q

6 MAJOR VIRAL ROUTES OF INFECTION?

A
  • RESPIRATORY TRACT
  • GI TRACT
  • GENITOURINARY TRACT
  • ENTERING THE BLOODSTREM DIRECTLY (WHEN AIDED BY SOME MECHANICAL EVENTS LIKE USE OF NEEDLES, A CUT, BITE OF AN INSECT, INTERCOURSE…)
  • EYES (WHEM A VIRION ON THE HANDS GAINS ENTRY WITH THE EYES BEING RUBBED, A NEONATE’S EYES CAN BE INFECTED WHEN PASSING THROUGH THE VAGINA DURING BIRTH..)
  • THROUGH SKIN
64
Q

IF A HUMAN IS ‘NAIVE’, WHAT DOES THAT INDICATE IN VIROLOGY?

A

THAT THEY HAVE NEVER BEFORE ENCOUNTERED THE VIRUS OR ITS COMPONENTS. SO THEY VIRUS HAS A HIGHER CHANCE OF CAUSING AN ACTIVE INFECION

65
Q

AFTER A VIRUS ENTERS HUMAN BODY, WHAT DOES IT NEED TO ENCOUNTER?

A

A SUSCEPTIBLE PERMISSIVE HOST CELL (DIRECTLY ASSOCIATED WITH THE NUMBER OF THOSE HOST CELLS AT THE SITE OF ENTRY, FURTHER INFECTION DEPENDS ON, AMONG OTHER FACTORS, THE ABUNDNACE OF RECEPTORS ON THOSE CELLS)

66
Q

WHT IS THE ‘INFECTIOUS DOSE’?

A

THE MINIMUM NUMBER OF VIRUSES NECESSARY TO CAUSE AN INFECTION, DEPENDS ON THE PRTICULAR VIRUS

67
Q

INFECTIOUS DOSES FOR INFLUENZA AND SMALLPOX?

A

INFLUENZ, ABOUT 800 INHALED VIRUSES

SMALLPOX, FEWER THAN 100 VIRUSES

68
Q

WHAT ARE THE TYPICAL NON-COVALENT!!!!!!!!!!! INTERMOLECULAR FORCES THAT HOLD THE SPIKE PROTEIN OF THE VIRUS AND THE HOST CELL RECEPTORS TOGETHER?

A

IONIC BONDS, HYDROGEN BONDS, LONDON DISPERSION FORCES (AK VAN DER WAALS INTERACTIONS)

69
Q

WHAT ALLOWS THE INTERMOLECULAR NONCOVALENT FORCES THAT JOIN VIRAL PROTEINS TO HOST CELL RCEPTORS TO OCCUR? WHAT KIND OF BINDING IS THIS?

A
  • THE STRONG FORCES CAN OCCUR BECAUSE OF SHAPE COMPLEMENTARITY (SHAPE COMPLEMENTARITY=ESSENTIAL FOR ATTACHMENT)
  • TIGHT BINDING SUCH AS THIS IS IRREVERSIBLE BECAUSE IT SOON TRIGGERS THE HOST CELL TO INTERNALIZE THE VIRUS
70
Q

WHAT CAN PREVENT THE HIV SPIKE PROTEIN FROM BINDING TO THE HOST CELL RECEPTORS?

A

PRESENCE OF HUMAN MILK OLIGOSACCHARIDES (HMOs) INGESTED WITH BREATSMILK

71
Q

HOW CAN cDNA BE UTILISED TO MAKE CELLS INTIALLY NON PERMISSIVE CELLS SUSCEPTIBLE TO INFECTION/ACQUIRE RECEPTORS VIRUSES CAN BIND TO? (because otherwise viruses would have quite a small library of viruses they can infect)

A

1) mRNA IS COLLECTED FROM THE PERMISSIVE CELLS (THE ONES WHO NATURALLY HAVE THE RECEPTORS THE VIRUS NEEDS)
2) mRNA IS THEN CONVERTED INTO A COLLECTION (LIBRARY) OF cDNAs (complementary DNA (cDNA) is DNA synthesized from a single-stranded RNA)
3) THE LIBRARY IS INTRODUCED INTO THE NON PERMISSIVE CELLS
4) SOME OF THE RECEPIENT CELLS THEN CONTAIN cDNA ENCODING THE NEEDED RECEPTOR PROTEIN
5) SOME OF THE PREVIOUSLY RESISTANT CELLS THUS BECOME SUSCEPTIBLE TO THE VIRUS BECAUSE THEY EXPRESS THE RECEPTOR PROTEIN FROM THE cDNA, WHICH CAN BE RCOVERED AND SEQUENCED IN ORDER TO IDENTIFY THE RECEPTOR PROTEIN

72
Q

WHAT IS AFFINITY CHROMATOGRAPHY? W=HOW CAN IT BE USEFUL IN VIROLOGY?

A

Affinity chromatography is a separation method based on a specific binding interaction between an immobilized ligand and its binding partner. Examples include antibody/antigen, enzyme/substrate, and enzyme/inhibitor interactions.
IN VIROLOGY, IT CAN BE USEFUL TO IDENTIFY A VIRUS RECEPTOR (A PROTEIN EXTRACT FROM PERMISSIVE CELLS, CONTINING THE VIRUS RECEPTO PROTEIN CAN BE OBTAINED—> THE EXTRACT CAN BE APPLIED INTO A CHROMATOGRAPHY COLUMN WHICH IS LOADED WITH INERT BEADS THAT HAVE THE VIRAL SPIKE PROTEIN COVALENTLY ATTACHED TO THEM —> AFTER APPLYING THE CELLULAR EXTRACT TO THE COLUMN, THE RECEPTOR BINDS TO THE SPIKE PROTEIN ON THE BEADS, WHILE ALL OF THE OTHER PROTEINS WASH THROUGH —> THE BEADS WITH BOUND RECEPTOR CAN THEN BE WASHED AND THE RECEPTOR CAN BE PURIFIED AND IDENTIFIED USING A VARIETY OF BIOCHEM TECHNIQUE)

73
Q

WHAT IS THE STRUCTURALY SIMPLEST ANTIBODY MADE BY HUMANS?

A

IgG ANTIBODY

74
Q

IgG ANTIBODY STRUCTURE?

A
  • A CONSTANT REGION (HEAVY CHAIN), Fc
  • A VARIABLE REGION (LIGHT CHAINS + EPITOPE BINDING SITE)
  • IN TOTAL, 4 SEPARATE POLYPEPTIDE CHAINS: 2 IDENTICAL LIGHT AND 2 IDENTICAL HEAVY CHAINS
75
Q

FUNCTIONING OF ANTIBODIES AS A RESPONSE TO VIRUSES?

A
  • AN ANTIBODY PHISICALLY OCCLUDES A RECEPTOR SO THAT THE VIRUS CANNOT ATTACH TO THE HOST CELL
    MONOCLONAL ANTIBODIES THAT BIND TO AN EPITOPE ON THE VIRAL SPIKE PROTEIN PREVENT THE VIRUS FROM GETTING BINDING TO ITS RECEPTOR
    ANTIBODIES CAN ALSO NEUTRALISE A VIRUS BY BLOCKING ITS ABILITY TO BIND TO A RECEPTOR (VIRUSES CAN END UP BEING COVERED WITH ANTIBODIES)
75
Q

FUNCTIONING OF ANTIBODIES AS A RESPONSE TO VIRUSES?

A
  • AN ANTIBODY PHISICALLY OCCLUDES A RECEPTOR SO THAT THE VIRUS CANNOT ATTACH TO THE HOST CELL
    MONOCLONAL ANTIBODIES THAT BIND TO AN EPITOPE ON THE VIRAL SPIKE PROTEIN PREVENT THE VIRUS FROM GETTING BINDING TO ITS RECEPTOR
    ANTIBODIES CAN ALSO NEUTRALISE A VIRUS BY BLOCKING ITS ABILITY TO BIND TO A RECEPTOR (VIRUSES CAN END UP BEING COVERED WITH ANTIBODIES)
76
Q

A 5 POINTED STAR SUROUNDE BY A CANYON IS A CHARACTERISTIC OF WHICH VIRUS STRUCTURE/

A

RHINOVIRUS

77
Q

NAME OF THE CELLULAR RECEPTOR FOR RHINOVIUS?

A

ICAM-1

78
Q

WHAT IS THE HOST RECEPTOR FOR INFLUENZA?

A
  • INFLUENZA DOESN’T ACTUALLZ BIND TO RECEPTORS BUT TO GLYCOCALYX ON THE SURFACE OF HUMAN RESPIRATORY TISSUE; CARBOHYDRATE SIALIC ACID, AKA NEURAMINIC ACID
79
Q

HOW MANY SPIKE PROTEINS DOES INFLUENZA HAVE + NAMES?

A

2: HEMAGGLUTININ AND NEURAMINIDASE SPIKES

80
Q

DESCRIBE THE VIRAL PENETRATION INTO A HOST CELL THROUGH RECEPTOR MEDIATED ENDOCYTOSIS

A
  • LIGANDS USUALLY BINDS TO A RECEPTOR
  • BINDING OF SEVERAL LIGANDS LEADS TO THEIR CLUSTERING
  • AFTER THEY CLUSTER, A CLATHRIN COAT VESICLE FORMS AND INTERNALISES THE RECEPTORS (CLATHRIN-COATED PITS)
  • AFTER INTERALISATION, THE CLATHRIN PROTEINS ARE RECYCLED AND THE EARLY ENDOSOME ACIDIFIES, TRIGGERING VIRAL UNCOATING
    VIRUSES USE THIS PROCES BY MIMICKING LIGAND BINDING, RESULTING IN VILUS INTERALISATION I.E. CELL ENTRY
81
Q

WHAT ARE CAVEOLINS AND HOW ARE THEY RELEVANT FOR VIRUSES?

A

In molecular biology, caveolins are a family of integral membrane proteins that are the principal components of caveolae membranes and involved in receptor-independent!!! endocytosis. They can facilitate viral entry into host cells —> after viruses are internalised they are moved as a component of CAVEOSOMES (components which contain molecules internalized by the caveolar endocytosis), and ultimately reach structures like ER

82
Q

DESCRIBE VIRAL ENTRY BY PHAGOCYTOSIS

A

SOME VIRUSES (E.G. KAPOSI’S SARCOMA VIRUS, FORMALLY KNOWN AS HUMAN HERPESVIRUS ) ENTER HOST CELLS THROUGH PHAGOCYTOSIS (Phagocytosis is a specific form of endocytosis by which cells internalise solid matter, including microbial pathogens), WHICH ULTIMATELY EXPOSES THE VIRION TO THE CONTENTS OF A PHAGOLYSOSOME, TRIGGERING UNCOATING (A process in which the viral capsid of a virus is removed, leading to the release of the viral genomic nucleic acid).

83
Q

RECEPTOR MEDIATED ENDOCYTOSIS?

A

Receptor-mediated endocytosis (RME), also called clathrin-mediated endocytosis, is a process by which cells absorb metabolites, hormones, proteins – and in some cases viruses – by the inward budding of the plasma membrane (invagination)

84
Q

VIRUS VS VIRION?

A

Definition
Virus: Virus is a small parasite that consists of a nucleic acid molecule covered by a protein coat.
Virion: Virion is the complete, infective form of a virus outside the host cell.

Intracellular/Extracellular
Virus: Virus is the intracellular structure.
Virion: Virion is the extracellular structure.

Shape
Virus: The shapes of a virus are helical, icosahedral, prolate, envelope, and complex.
Virion: Most virions are spheroidal or rod-shaped.

Generally, virus refers to a type of nucleoprotein and virion refers to the complete particle that is infectious. Therefore, the main difference between virus and virion is the role they play during infection.

85
Q

EXAMPLES OF VIRAL PENETRATION MECHANISMS?

A
  • RECEPTOR MEDIATED ENDOCYTOSIS
  • PHAGOCYTOSIS
  • RELEASE OF GENOME THROUGH PORE FORMATION (E.G. PICORNAVIRUSES)
  • PENETRATION THROUGH MEMBRANE FUSION (E.G. HIV, INFLUENZA)
86
Q

HOW CAN VIRUSES USE THE CYTOSKELETON OF HOST CELLS?

A
  • THEY CAN USE IT FOR TRANSPORT WITHIN THE CELL
  • USING E.G. MICROTUBULES AND THEIR ASSOCIATED MOTOR PROTEINS (DYNEINS MOVE CARGO SUCH AS VIRUSES TOWARDS THE - END OF THE MICROTUBULE AND THEREFORE TOWARD THE NUCLEUS)
87
Q

HOST RECEPTORS FOR ANIMAL VIRUSES ARE USUALLY WHICH TYPE OF PROTEIN?

A

GLYCOPROTEIN

88
Q

VIRAL PENETRATION DEFINITION?

A

THE RELEASE OF THE VIRION OR PARTS OF THE VIRION INTO THE INTERIOR OF A HOST CEL

89
Q

WHERE DO MOST DNA VIRUSES HAVE TO DELIVER THEIR GENOMES AND HOW?

A
  • INTO THE HOST CELL NUCLEUS, TYPICALLY THROUGH INTERACTIONS WITH A NUCLEAR PORE COMPLEX
90
Q

PENETRATION BY ENVELOPED VIRUSES? HIV + INFLUENZA EXAMPLES

A
  • USE FUSION PEPTIDES TO CATALYSE FUSION WITH HOST MEMBRANES
  • FUSION PEPTIDES ARE COMPONENTS OF SPIKE PROTEINS THAT ARE INACTIVE UNTIL ACTIVATED BY A CASCADE OF PROTEIN-PROTEIN INTERACTIONS (HIV) OR LATE ENDOSOME ACIDIFICATION (INFLUENZA)
  • VIRUSES CAN DELIVER JUST THE GENOME, PARTS OF THE CAPSID ACCOMPANYING THE GENOME ETC
91
Q

OUTCOMES OF INFECTION BY DNA VIRUSES?

A
  • LYTIC INFECTION
  • CELLULAR TRANSFORMATION
  • LATENT INFECTION
92
Q

HOW DO MOST DS DNA VIRUSES REGULATE GENE EXPRESSION?

A

BY RELYING ON HOST MACHINERY FOR GENE EXPRESSION

93
Q

EXPLAIN: ‘CAPPING AND SPLICING ARE CO-TRANSCRIPTIONAL’

A

AS THE PRE-MRNA EMERGES FROM THE TRANSCRIPTION MACHINERY, CAPPING AND SPLICING FACTORS MODIFY THE RNA DURING TRANSCRIPTION ELONGATION

94
Q

HOW IS TRANSCRIPTION INITIATED?

A
  • NUCLEOSOMES NEED TO BE REMOVED FROM THE PROMOTER IN ORDER FOR THE TRANSCRIPTION MACHINERY ASSEMBLE
  • THE MEDIATOR IS A VERY LARGE COMPONENT OF THE TRANSCRIPTION MACHINERY THAT INTEGRATES ACTIVATING AND REPRESSING SIGNALS TO CONTROL THE INITIATION OF TRANSCRIPTION BY POLL II (RNA polymerase II (RNAP II and Pol II) is a multiprotein complex that transcribes DNA into precursors of messenger RNA (mRNA) and most small nuclear RNA (snRNA) and microRNA. It is one of the three RNAP enzymes found in the nucleus of eukaryotic cells)
95
Q

WHAT ARE THE SMALLEST DSDNA VIRUSES INFECTING ANIMAL CELLS?

A

POLYOMAVIRUSES

96
Q

miRNA (SMALL REGULATORY RNA) IS EXPRESSED AT WHICH POINT DURING VIRAL INFECTION?

A

LATE DURING INFECTION

97
Q

SARS COV 2 VIRION DIAMETER?

A

120 nm

98
Q

CORONAVIRUS STRUCTURAL PROTEINS?

A
  • ENVELOPED VIRUS HAS SPIKES COMPOSED OF THE S PROTEIN
  • 2 TRANSMEMBRANE PROTEINS: E AND M
  • THE NUCLEOCAPSID PROTEIN ‘N’, THAT IS BOUND TO THE GENOME FORMING A HELICAL CONFORMATION INSIDE THE ENVELOPE
99
Q

CELLS INFECTED WITH CORONAVIRUS CONTAIN A MINIMUM OF HOW MANY VIRAL RNAs?

A

10

100
Q

STRUCTURE OF TOBACCO MOSAIC VIRUS (TMV)

A
  • TMV VIRIONS ARE COMPOSED OF 2,130 IDENTICAL CAPSOMERES ARRANGED IN A HELICAL PATTERN SURROUNDING A SINGLE GENOME RNA MOLECULE
101
Q

EXAMPLES OF SITES OF VIRAL ASSEMBLY?

A

CYTOPLASM (BACTERIOPHAGES, PICORNAVIRUSES, REOVIRUSES)
NUCLEUS ( POLYOMAVIRUSES, PAPILLOMAVIRUSES, ADENOVIRUSES)
PLASMA MEMBRANE (RETOVIRUSES AND RHABDOVIRUSES)
ENDOPLASMIC RETICULUM (CORONAVIRUSES AND POXVIRUSES)
NUCLEUS AND CELLULAR MEMBRANES (HERPESVIRUS AND INFLUENZA VIRUS)

102
Q

WHAT IS THE SITE OF ASSEMBLY FOR CORONAVIRUSES?

A

ENDOPLASMIC RETICULUM

103
Q

HOW ARE SPIKE PROTEINS ADDED ONTO VIRUSES DURING ASSEMBLY?

A
  • VIA ENDOMEMBRANE TRAFFICKING OF VESICLES CONTAINING VIRAL SPIKE PROTEINS
  • VESICLES MOVE PROTEINS FROM THE ROUGH ER THROUGH THE GOLGI APPARATUS
  • FROM THE GA. VESICLES MOVE TO THE PLASMA MEMBRANE AND FUSE WITH IT, SO THE PROTEINS FROM THE VESICLES BECOME PART OF THE MEMBRANE
  • THE PORTIONS OF THE VIRUS SPIKE PROTEINS THAT HAD BEEN INSIDE THE LUMEN OF THE ER BECOME THE OUTSIDE (DISTAL) SURFACE OF THE VIRAL ENVELOPE
104
Q

SEQUENTIAL VIRAL ASSEMBLY?

A

AN EMPTY PROCAPSID ASSEMBLES FIRST AND IS SUBSEQUENTLY FILLED WITH THE GENOME (USUALLY OCCURS WITH SPHERICAL CAPSIDS)

105
Q

CONCERTED VIRAL ASSEMBLY?

A

THE CAPSID AND THE GENOME ASSEMBLE TOGETHER SO THAT THERE ARE NO EMPTY PROCAPSDS: INSTEAD THERE IS A NUCLEOPROTEIN COMPLEX (E.G. RABIES, INFLUENZA, PICORNAVIRUSES)

106
Q

WHAT ARE CHAPERONS?

A

PROTEINS THAT MAKE PROTEIN FOLDING FASTER AT THE EXPENSE OF ATP (IMPORTANT FOR VIRUS ASSEMBLY, VIRUSES USE HOST CHAPERON PROTEINS)

107
Q

WHAT ARE SCAFFOLDS?

A

PROTEINS THAT ARE NEEDED FOR PARTS OF THE VIRUS TO ASSEMBLE BUT ARE NOT FOUND IN A MATURE VIRION (VIRUS DERIVED)

108
Q

EXAMPLE OF A VIRUS THAT ASSEMBLES A NUCLEOCAPSID OR CAPSID PRIOR TO ACQUIRING AN ENVELOPE?

A

INFLUENZA, PICORNAVIRUSES

109
Q

EXAMPLE OF A VIRUS THAT ACQUIRES THE ENVELOPE AND ASSEMBLES CAPSOMERES WITH THE GENOME SIMULTANEOUSLY?

A

HIV

110
Q

vRNPs are?

A

VIRUS NUCLEOPROTEINS

111
Q

INFLUENZA VIRUS ENVELOPE STRUCTURE?

A
  • ENVELOPE CONSISTING OF A LIPID BILAYER INCLUDING 4 VIRAL PROTEINS: THE HA SPIKE, THE NA SPIKE AND THE TWO MATRIX PROTEINS M1 AND M2
  • INTERNAL TO THE LIPID BILAYER ARE EIGHT DIFFERNENT vRNPs, EACH CONSISTING A SINGLE DIFFERENT - SENSE RNA BOUND TO OTHER PROTEINS
112
Q

RELEASE OF PHAGES FROM HOST CELLS BY LYSIS: WHAT ARE THE KEY PROTEINS?

A

HOLIN: AGGREGATES IN THE PLASMA MEMBRANE, AND WHEN IT BECOMES VERY NUMEROUS REARRANGEMENT OCCURS LEADING TO FORMATION OF LARGE AQUEOUS PORES THROUGH THE PLASMA MEMBRANE
ENDOLYSIN: CAN ONLY ENTER THE PERIPLASM AFTER HOLIN CREATES THE AQUEUOUS PORES —> AFTER ENTERING THE PERIPLASM, IT BINDS TO PEPTIDOGLYCAN AND DEGRADES THE MACROMOLECULE
SPANIN: AFTER HOLIN AND ENDOLYSIN ACTIVITY, SPANIN FUSES THE OUTER MEMBRANE TO THE PLASMA MEMBRANE, FORMING LARGE CHANNELS THROUGH WHICH PHAGES ESCAPE (CREATES CHANNELS)

113
Q

WHEN BUDDING FOM HOST CELS, HIV USES WHICH MACHINERY?

A

ESCRT MACHINERY (CREATES MULTIVESCULAR BODIES)

114
Q

WHICH STRUCTURE IN THE EUKARYOTES IS ESSENTIAL FOR BRINGING VIRUS COMPONENTS TOGETHER (AS DIFFUSION WOULD BE TOO SLOW)?

A

THE CYTOSKELETON

115
Q

WHICH VIRUS SERVES AS A MODEL FOR EXIT FROM HOST CELLS WITH MULTIPLE EXTERIOR LAYERS?

A

THE LAMBDA VIRUS (BACTERIOPHAGE)

- MECHANISM OF 3 PROTEINS: HOLIN, ENDOLYSIN AND SPANIN

116
Q

EXAMPLE OF VIRUSES THAT ESCAPE HOST CELLS BY WEAKENING THE CYTOSKELETON, ENDING IN LYSIS?

A

ADENOVIRUSES

117
Q

HIV GENETIC MATERIAL?

A

SINGLE STRAND POSITIVE SENSE RNA

118
Q

WHAT IS SMALLPOX VACCINE MADE FROM?

A

The vaccine is made from a virus called vaccinia, which is a poxvirus similar to smallpox, but less harmful. The smallpox vaccine contains live vaccinia virus, not a killed or weakened virus like many other vaccines. For that reason, people who are vaccinated must take precautions when caring for the place on their arm where they were vaccinated, so they can prevent the vaccinia virus from spreading.

The vaccine does not contain the smallpox virus and cannot give you smallpox.

For most people with healthy immune systems, live virus vaccines are effective and safe. Sometimes a person getting a live virus vaccine experiences mild symptoms such as rash, fever, and head and body aches.
—> LEAVES A SCAR

(Other live virus vaccines currently used include measles, mumps, rubella, and chickenpox.)

119
Q

EXAMPLE OF A VIRUS THAT HAS PRIMARLY DNA BASED GENOME, BUT ALSO INCLUDES A BIT OF RNA

A

HEP B

120
Q

RETROVIRUSES?

A

A retrovirus is a virus that uses RNA as its genetic material. When a retrovirus infects a cell, it makes a DNA copy of its genome that is inserted into the DNA of the host cell. There are a variety of different retroviruses that cause human diseases such as some forms of cancer and AIDS.

Retroviruses are a family of viruses that are grouped together based on how they are structured and how they replicate within a host. Besides human immunodeficiency virus (HIV), the virus that causes AIDS, there a two other retroviruses that can cause human illness. One is called human T-lymphotropic virus type 1 (HTLV-1) and the other is called human T-lymphotropic virus type 2 (HTLV-II). Both of these viruses are transmitted between people through sexual contact, infected blood or tissue exposure, or during pregnancy or childbirth from an infected person to their child.

121
Q

WHICH CLASS IN THE BALTIMORE SCHEME ARE RETROVIRUSES?

A

VI

122
Q

SEGMENTED GENOME?

A

A viral genome fragmented into two or more nucleic acid molecules. For example, the alfalfa mosaic virus has four different RNA segments, each packaged in a different virion. Successful infection requires that at least one RNA of each type enters the cell. Such a virus is said to be heterocapsidic. If all fragments of a segmented genome are present in the same virion (e.g., influenza virus!!!!!!!!!!!!!!!!), the virus is said to be isocapsidic.

123
Q

HOW DOES INFLUENZA VIRUS ENTER HOST CELLS?

A

IT IS ENTERNALISED BY ENDOCYTOSIS

124
Q

POLY A TAIL?

A

The poly-A tail is a long chain of adenine nucleotides that is added to a messenger RNA (mRNA) molecule during RNA processing (immediately after a gene in a eukaryotic cell is transcribed, the new RNA molecule undergoes several modifications known as RNA processing) to increase the STABILITY of the molecule

125
Q

MAIN VIRAL PENETRATION AND UNCOATING STRATEGIES?

A

A) RELEASE OF VIRAL GENOME INTO THE CYTOPLASM THROUGH A PORE

B) FUSION OF ENVELOPED VIRUS AT THE PLASMA MEMBRANE, RELEASING THE NUCLEOCAPSID INTO THE CYTOPLASM AND LEAVING VIRAL SPIKE PROTEINS ON THE CELL SURFACE

C) ENDOCYTOSIS OF A VIRUS FOLLOWED BY RELEASE OF THE NUCLEOCAPSID INTO THE CYTOPLASM; NO VIRAL PROTEINS LEFT ON THE CELL SURFACE

126
Q

ADENOVIRUSES?

A

Adenoviruses are medium-sized, nonenveloped viruses with an icosahedral nucleocapsid containing a double-stranded DNA genome.

Adenoviruses can cause a wide range of illnesses such as

common cold or flu-like symptoms
fever
sore throat
acute bronchitis (inflammation of the airways of the lungs, sometimes called a “chest cold”)
pneumonia (infection of the lungs)
pink eye (conjunctivitis)
acute gastroenteritis (inflammation of the stomach or intestines causing diarrhea, vomiting, nausea and stomach pain)

127
Q

CAP SNATCHING?

A
  • DONE BY E.G. INFLUENZA A VIRUS
    The first step of transcription for some negative, single-stranded RNA viruses is cap snatching, in which the first 10 to 20 residues of a host cell RNA are removed (snatched) and used as the 5′ cap and primer to initiate the synthesis of the nascent viral mRNA.
128
Q

ANTIGENOME?

A

The complementary strand of RNA from which the genome of a virus is constructed.

INF (40 decks)

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