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Virology Exam 3 > Study Guide > Flashcards

Study Guide Flashcards

1
Q

What is the occurrence of Influenza related pneumonia among infants, children and adults?

A

*Influenza causes PNA in children and adults more than other respiratory viruses.
*In infants, RSV causes PNA more commonly than the flu does.

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2
Q

Who is at risk for life threatening pneumonia due to the respiratory syncytial virus (RSV)?

A

*Infants and young children (infects by age 4)

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3
Q

Study data and trends in the graph depicting total respiratory infections of known etiology

A

*Rhinovirus- 38.5%
*Parainfluenza- 16.9%
*Influenza- 11.9%
*RSV- 5.9%
*Group A beta-hemolytic streptococci-13.3%
*Mycoplasma & other- 4.7%
*Adenoviruses- 4.5%
*Enteroviruses- 4.3%

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4
Q

Sneeze versus a cough

A

*Sneeze- releases 20K droplets
*Due to forcefulness and depth from which sneeze arise means they have more droplets therefore GREATER shedding
*Coughing releases less amount of droplets vs sneezing.

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5
Q

What best describes the structure and infectivity of the Rhinovirus?

A

*Rhinovirus is a small, naked, positive sense RNA virus

*Due to the nature of rhino being an RNA virus, it triggers a significant interferon response.

*The convergence of VP1, VP2, and VP3 produces Canyon, the VAP of rhino.
*This area is highly conserved because of its advantage being inaccessible to antibodies.

*Rhinovirus is highly infectious, as its RNA genome is quickly translated to polyprotein. There are 400,000 molecules of RNA per cell, and these are released by cell lysis.

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6
Q

What aspect of the Rhinovirus viral attachment protein is related to immune evasion?

A

*The inaccessibility of Canyon to antibodies is related to the way rhinovirus evades the host immune system.

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7
Q

What is characteristic of Rhinovirus pathogenesis?

A

*IFN production is what causes the aches and pains that are felt during an infection with rhinovirus. This is a systemic effect that is produced as a result of infection with rhino.

*The upper respiratory tract is a perfect temperature for the virus to thrive in (33 C)
- Sore throat
- Runny nose → Bradykinin and histamine release
- 500 to 1000 infectious particles present in 1mL of nasal secretions
- Interferon production

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8
Q

What is the treatment for Rhinovirus?

A

*OTC products for symptoms (anti-histamines)
*There are also zinc-lozenges - shortens duration of replication
**Experimental canyon binding molecules
-Canyon binding molecules were discontinued from the market as they were interfering with birth control.

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9
Q

Coxsackievirus A21 versus Enterovirus 70

A

*Coxsackievirus A21 - Upper respiratory infection
*Enterovirus 70 - acute hemorrhagic conjunctivitis

*Coxsackie virus is an enterovirus that causes URI’s that commonly present with cold-like symptoms and fever.
*Enterovirus 70, a naked virus, can cause acute hemorrhagic conjunctivitis.

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10
Q

Pathogenesis of a Parainfluenza infection?

A

-Infection ranges from mild cold-like symptoms to lower respiratory tract infections
-Commonly the causative agent of croup (laryngotracheobronchitis)
-Can cause syncytia and cell lysis
-CMI clears infection but contributes to disease

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11
Q

General aspects of the Coronavirus?

A

-Enveloped RNA virus with club shaped glycoproteins resembling solar corona
-Replicates in the cytoplasm
-Infects epithelial cells of the URT
-Optimal temperature for replication is 33 to 25 C
-Can complicate pre-existing pulmonary diseases (asthma or bronchitis)
*Enveloped RNA virus with club shaped glycoproteins around the surface.

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12
Q

What respiratory region is associated with infection by Parainfluenza?

A

**The lower respiratory region consisting of the larynx, trachea, bronchi, and bronchioles.
* This is why it is called laryngotracheobronchitis infection and it should be noted that it is more dangerous in children due to their smaller airways.

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13
Q

What cytopathology is associated with RSV infection?

A

*-Syncytial formation
-Invades superficial layers of epithelial cells and can cause inflammation of narrow bronchiole tubes

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14
Q

Who is at risk for the metapneumovirus?

A

*Children under 6 years (96% of all cases in 2001 were isolated from children under 6)

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15
Q

Many viral infections trigger a strong interferon response. What is an exception?

A

**RSV
*The absence of IFN production in an infection with RSV is why adults kissing babies is dangerous as they are shedding the virus without knowing it due to being asymptomatic.

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16
Q

What best describes the structure and pathogenesis of the Influenza virus?

A

*Structure
- Enveloped RNA
- Segmented genome
- VAP: HA
- Glycoproteins NA
-Negative sense ssRNA

*Pathogenesis
-Aerosol inoculation of virus results in replication in respiratory tract causing desquamation of mucus-secreting and ciliated cells producing INFLUENZA syndrome
-Influenza syndrome may cause: secondary bacterial infection turning into PNA
-Primary viral PNA
-CNS and muscle involvement
-This alerts antibody productions, T-cell responses, and interferon induction

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17
Q

What is representative of genetic drift and genetic shift in Influenza genetics?

A

*Genetic drift is LONG duration of time to see changes -> results of compilation of mutations over years
-change due to nucleotide substitutions (slowly changes over the years)

*Genetic shift is SHORT duration of time to see change -> 1 year to the next associated with reassortment
-change due to reassortment (one year or less)

***Both specifically related to HA and NA glycoproteins in influenza

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18
Q

How is the flu vaccine designed for the 2022-2023 season in the summer of 2022 preceding the “flu season?”

A
  • It’s based on the predominant strains from the last flu season.
  • Will always have 2 A and at least 1 B.
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19
Q

What facilitates the endosomal escape of Influenza during the penetration and uncoating process?

A
  • Hemagglutinin (trimer springs opens ends up in lipid bilayer) -> VAP

**This has to do with the conformational change that occurs in HA which facilitates the fusion inside of the cytoplasm and the constituents of the virus are then dumped into the cytoplasm and eventually end up in the nucleus.
Also note drop in endosomal pH that triggers this conformational change

*(As the endosome becomes acidified, protons are pumped to the inside of the endosome all leading to changes taking place with the proteins that are connected to the genome.)
Hence why proton pump inhibitors used to be used as treatment for the flu.

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20
Q

What is the molecular target of Tamiflu?

A

**Neuraminidase

*NA aids in the facilitation of viral spread from cell to cell thus when targeted further spread of the virus is prevented.

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21
Q

What best describes the “back boost’ from a vaccine?

A

-reinvigoration of the antibodies from a previous vaccine/exposure

-“The inactivated vaccine elicits HI antibodies against viruses that vaccines have encountered over their lifetime, not just the antigens in the vaccines
Additional protection against the virus is added when vaccinated because the vaccine aids in the formation of new memory cells which could be preventative against a different strain of the virus, for example, influenza.

Memory T cells and B cells are associated with immunologic imprinting.

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22
Q

How do vaccines affect memory cells and naïve B cells?

A

*“An unbiased antibody repertoire analysis revealed that the inactivated vaccine elicits antibody production from memory and naive B cells.”

*Response comes from MEMORY

23
Q

What is immunologic imprinting?

A

-*Varies between generation to generation because the circulating Influenza A viruses in childhood differ
**Whatever infections an individual is exposed to at a young age creates a predominate significant memory that allows subsequent vaccination in infection to influence

24
Q

HPV and its ease of transmissibility?

A

*HPV- one of the most prevalent STDs in the world
*At least 20 million people in the US infected with HPV
*Direct contact through small breaks in the skin or mucosa
*Sexual contact (sexually transmitted disease) for certain virus types
*Passage through infected birth canal for laryngeal papillomas
**HPV is easily transmitted and is considered the number one sexually transmitted entity as it can be transmitted via fomites, direct contact, etc.

25
Q

Persistence of HPV in the skin … where does it replicate in the skin?

A

*Squamous epithelium and then in mucus membranes
**HPV replicates in BASAL LAYER

26
Q

What human cellular tumor suppressor protein is affected by certain strains of HPV expressing the E6 and E7 gene products?

A

**p53; Rb product

27
Q

What is cellular cytopathology of koilocytosis?

A

Koilocytes may have the following cellular changes:
-Nuclear enlargement (two to three times normal size)
-Irregularity of the nuclear membrane contour
-Hyperchromasia
- a clear area around the nucleus known as perinuclear halo

**Koilocytotic cells will appear with perinuclear cytoplasmic vacuolization and nuclear enlargement.

28
Q

What HIV structure is directly related to its mode of transmission?

A

-2 surface proteins on the envelope– gp120 and gp41 ->Antigenic and facilitate attachment with CD4+

-Cone/Cylindrical-shaped nucleocapsid core containing major capsid protein p24

-Matrix protein (p17) – present when capsid and the envelope and essential for the process of virus assembly during replication

29
Q

What molecule is associated with the attachment and penetration of HIV into its host cells?

A

**gp41 attaches to CD4+ T cells
*Gp41 is the viral transmembrane protein that facilitates viral fusion to the host cell.

30
Q

HIV receptors and tropism.

A

-R5 strains preferentially bind to CC chemokine receptor-5 (CCR5) co-receptors that are present on both monocytes and CD4+ T cells.

-R4 strains preferentially bind to CXC chemokine receptor-4 (CXCR4) co-receptors (predominantly on CD4+ T cells).

*Tropism: the availability of virus receptors on the surface of a host cell
**X4-tropic strain
**R5-tropic-only strain

31
Q

What defines the different stages of HIV infection in a patient?

A
  1. Initial infection: cells infected by HIV may be killed by viral replication or by virus-specific immune effector cells- CTL, ADCC
  2. Chronic phase of infection: after a few months there is a balance among virus infection, immune effector mechanisms and the number of cells available for infection. Patient is generally asymptomatic: in the the chronic phase
  3. Viral replication “set-point”: generally determines the rate to disease progression

-“stage of disease correlates with spread of HIV from initial site of infection to lymphoid organs throughout body”
**This can be monitored by levels of CD4+ T cells and HIV RNA present in serum

32
Q

What is characteristic of immunodeficiency (AIDS)?

A

**Characteristic to AIDS (full-blown) is the:
-CD4+ T cell count decreasing to below 200/mm3 and having notably increased virus levels in the blood.
-There can also be the occurrence of indicator diseases such as Kaposi sarcoma, thrush, severe CMV diseases, pneumocystis pneumonia..etc.
-There can also be dementia related to AIDS due to the infection of macrophages and microglial cells or from opportunistic infection(s).

33
Q

During the 7 year (84 months) progression from infection to AIDS … what happens with antibodies, HIV levels and Tcells?

A

**Reductions in the numbers of CD4 T cells may result from direct HIV-induced cytolysis, cytotoxic T-cell-induced immune cytolysis, leading to a rapid terminal differentiation and death of T cells.
**Targeting of CCR5-expressing T cells depletes the gut-associated lymphoid tissue of CD4 T cells.
Level of CD4+ T cells drops below 200/mm3 and continues to decrease to near zero while the levels of virus in the blood continue to increase until death. **Antibodies begin to develop approximately 4-8 weeks after infection with HIV and continue to persist throughout infection to death.

** T-cell levels initially decrease followed by a rebound before starting decline again (down up down). HIV RNA spike following infection and decrease during the acute illness phase.. followed by a plateau in the latent phase with an increase in the AIDS phase (up down up).

34
Q

What kind of drug therapy is used to treat HIV infections?

A

-Nucleoside reverse transcriptase inhibitors - NRTI
-Nucleotide RT inhibitors
-Non-nucleoside RT -Inhibitors - NNRTI
-Protease inhibitors - ending in -NAVIR
-Entry/Fusion inhibitors
-Integrase inhibitors
-CCR5 inhibitors
***Can be called active retroviral therapy (ART) or the combination therapy can be called highly active anti-retroviral therapy (HAART).

35
Q

What is associated with the disease caused by Coltivirus?

A

*Colorado Tick Fever
- Hemorrhagic disease -> vascular endothelial and vascular smooth muscle
- Neuronal infection -> meningitis, encephalitis
- Hepatitis, epididymo-orchitis, pericarditis, myocarditis and pneumonitis
- Ticks
- Infects erythrocyte precursors and persists in mature RBCs
**Clinical symptoms include biphasic fever and conjunctivitis as well as a maculopapular or petechial rash.

36
Q

What is the respective vector and host for most alphaviruses and flaviviruses?

A

*Alphaviruses (aka togavirus)
-Vector: MOSQUITOS- Aedes, Culex, Culistea
-Host: mainly birds, also horses, monkeys, and humans

*Flaviviruses
-Vector: MOSQUITOS & TICKS - Aedes, Culex, Ixodes and Dermacentor ticks
-Host: Humans, monkeys, birds, pigs, small mammals

**Both are under broad category of arboviruses and have a mosquito or tick vector and then generally there is some type of host.

37
Q

Arboviruses and farm animals.

A
  • Family of arboviruses
    A. Alphaviruses: Sindbis, Semliki Forest, Venezuelan equine encephalitis, Eastern equine encephalitis, Western equine encephalitis, Chikungunya
    B. Flaviviruses: Dengue, Yellow Fever, Japanese encephalitis, West Nile encephalitis, St. Lois encephalitis, Russian spring-summer encephalitis, Powassan encephalitis

-Vectors: Ticks and mosquitos
-Hosts: Birds, Rodents, Horses, Humans, Monkeys, Pigs, and small mammals

-Incidence of disease correlates with vector, host, and location
Western equine encephalitis, eastern equine encephalitis, and venezuelan equine encephalitis are all arboviruses that the dead-end hosts can either be humans or horses but these are MORE common in horses than humans.

WNV causes flu-like symptoms, encephalitis, and hepatitis. Host for WNV is birds and vector is Culex mosquito. (TA said something about knowing info about WNV).

38
Q

What is different about Hantavirus with other Bunyaviridae?

A

-No insect vector, infects rodents
-Infects lungs → hantavirus pulmonary syndrome

**Hantavirus has no insect vector and the hosts are rodents. Hantavirus can cause adult respiratory distress syndrome and can be very dangerous leading to respiratory failure and even death. It is spread through close contact or aerosolized rodent urine.
**Bunyaviridae have an insect vector, which are arthropods. Bunyaviridae are more or less associated with febrile illness, febrile rash, and sometimes encephalitis.

39
Q

What is the pathogenesis of Ebola?

A

*Ebola virus enters the patient through mucous membranes -> breaks in the skin or parenterally -> infects many cell types -> migrates from initial infection site to regional lymph nodes and to liver, spleen, and adrenal glands.
**Pathogenesis includes tissue necrosis in parenchymal cells (liver, spleen, lymph nodes, and lungs), massive hemorrhaging, edema, and hypovolemic shock.

40
Q

What is the major vector for disease for arenaviruses?

A

*is Rodent infections, zoonotic to human

41
Q

Know the structures of all the hep viruses … e.g. enveloped, DNA

A
  1. Hep A: Capsid, RNA
    naked, icosahedral symmetry, positive sense ssRNA
  2. Hep B: Enveloped, DNA
  3. Hep C: Enveloped, RNA
    icosahedral symmetry, positive sense ssRNA
  4. Hep D: Enveloped, circular RNA, Tiny RNA genome (ribozyme)
  5. Hep E: Capsid, RNA
    naked, icosahedral symmetry, positive sense ssRNA
42
Q

Hepatitis B Virus and the production of large amounts of S protein

A

**S protein plays a crucial role in viral entry into host cells as it is a part of the viral envelope and helps the virus attach to and enter hepatocytes.
*S protein also helps the virus to evade immune detection by producing large amounts of S protein and diverting the immune response away from other viral elements such as the core protein.
*The S protein is also a primary target of the HepB vaccine as it contains a recombinant form of the S protein to stimulate the immune system to produce Ab’s against S protein to provide immunity against HBV infection.

**The reverse transcriptase process after transcription in the nucleus is likely why this ends up spitting out so many small non-infective proteins - the reverse transcriptase can’t keep up with it.

43
Q

Generally, when is the Hepatitis B vaccine first administered and why?

A

*Generally given w/in 24 h of birth
*Why: Hep B can be passed from mothers blood to baby, given to prevent an infection if exposed.

44
Q

Acute hepatitis

A

*Acute hepatitis is generally worse than chronic where acute infections produce more symptoms.
*The typical symptoms of acute hepatitis include fatigue, anorexia, nausea, vomiting, and high aminotransferase values and hyperbilirubinemia.
*Acute infection can be caused by HAV, HBV, or HCV and can show icteric symptoms such as jaundice and release of enzymes but usually results in resolution. *HAV is most common cause of acute hepatitis infection and acute infection is most associated with the development of fulminant hepatitis.

45
Q

Chronic Hepatitis

A

*Chronic hepatitis is commonly associated with HBV and HCV.
*There is a limited CMI response with chronic infection and the disease is associated with mild symptoms that continue for years and years.
*If delta agent coinfects with HBV, this can give rise to fulminant hepatitis.
*HBV and HCV can lead to primary hepatocellular carcinoma and cirrhosis following chronic infection. *HCV is the most common cause of chronic hepatitis and chronic hepatitis is most associated with cirrhosis of the liver due to the occurrence of long-term damage.

46
Q

What is associated with fulminant hepatitis?

A

*HAV and HBV are the two hepatitis viruses associated with causing fulminant hepatitis.
*There is an 80% mortality rate for fulminant hepatitis cases and fulminant hepatitis often results in liver failure and sometimes encephalopathy.
*Fulminant hepatitis is defined by the rapid onset of liver failure within a short period, usually within a few weeks after the initial symptoms of acute hepatitis.
*- Chronic hepatitis B infection and comes across delta agent causes Hep D causing fulminant hepatitis
- Acute liver failure in the setting of hepatic encephalopathy

47
Q

Hepatitis A infection pathogenesis

A

*Pathogenesis:
1) Enters blood through oropharynx or GI
2) IF localizes to hepatocytes and Kupffer
3) Large amounts released in bile and stools 10 days before jaundice or Ab
4) Cytotoxic T cells, Ab, complement, Ab-dependent cellular cyto facilitate clearance (Symptoms and liver pathology)
5) Following clearance - Lifelong Immunity
6) No chronic infection
7) No association with hepatic cancer

48
Q

Hep A infection epidemiology

A

*Epidemiology:
-40% of acute hepatitis cases
-Inapparent but productive infections
A. 90% of infected children
B. 25 to 50% of infected adults
-Spread fecal-oral route
-Contaminated water
-Dirty hands (daycare center)
-Food (restaurants)

49
Q

Hep A infection clinical syndromes

A

*Clinical syndromes:
-Similar to HBV
-Result of Immune-mediated liver damage
-Disease milder in children
-15 to 50 days after exposure: fever, fatigue, nausea, loss of appetite, RUQ
-4 to 6 days later icteric phase
-2/3 adults jaundice . . . 1/5 to 1/10 children
-Virus shedding occurs 14 days prior to symptoms

50
Q

Hepatits A infection

A

*HAV infection is the most common cause of acute hepatitis infection in the US.

HAV spreads by fecal-oral route. 15-50 days after exposure to the virus, an individual may experience fever, fatigue, nausea, and loss of appetite.

*Then there is an icteric phase of jaundice, pale skin, and dark urine. Resolution occurs unless fulminant hepatitis develops.

51
Q

Which hepatitis viruses are associated with cancer?

A

Hep B and Hep C

52
Q

Vaccines and hepatitis viruses

A

*HAV vaccine is an inactivated vaccine administered as 2 intramuscular doses around 6 months to 1 year apart. Coffman says he feels that pretty much everyone should be vaccinated against HepA.

*HBV vaccine is a recombinant vaccine where the S antigen is purified, meaning a subunit of HBsAg (HBV S protein antigen) is used and it is administered in 3 IM doses. This also provides protection against the delta, or HDV strain.

53
Q

What leads to cirrhosis?

A

The liver can restore, or regenerate, itself.
**Cirrhosis is directly caused by diffuse damage to hepatic parenchymal cells where there is nodular regeneration and fibrosis.

*This disturbs the normal architecture of the liver and interrupts the blood flow leading to scarring, or cirrhosis, of the liver.

Virology Exam 3 (1 decks)

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