Fungi & Virus III

1. Q: What are the three major outcomes of viral infections in host cells?

A:

• Acute infection

• Persistent/chronic infection

• Latent infection

2. Q: What happens during an acute viral infection? Give an example.

A: The virus replicates rapidly and typically causes death of the host cell. Examples: influenza and SARS-CoV-2.

3. Q: What happens during a persistent (chronic) viral infection? Give examples.

A: The virus continuously replicates over a prolonged period without immediately killing the host cell. Examples: HIV and hepatitis C virus (HCV).

4. Q: What happens during a latent viral infection?

A: The viral genome persists in the host cell with minimal or no viral gene expression. The virus can reactivate later.

5. Q: What can trigger reactivation of a latent virus? Give examples of latent viruses.

A: Environmental stress or changes in immune status. Examples:

• Herpes simplex virus (HSV)

• Epstein-Barr virus (EBV)

• Varicella-zoster virus (VZV)

6. Q: What are the four major ways viruses can damage or alter host cells?

A:

• Lysis: Damage to the plasma membrane causes loss of cell integrity.

• Anergy/dysfunction: Disrupts cell signaling and responsiveness.

• Apoptosis: Alters programmed cell death.

• Transformation: Alters cells so they lose normal growth control.

7. Q: What is viral transformation, and what can it lead to?

A: Viral transformation occurs when viral infection alters a cell's genetic material and normal growth regulation, potentially leading to cancer.

8. Q: What are oncoviruses? Give examples.

A: Viruses that can contribute to cancer through cellular transformation. Examples include:

• EBV

• Certain HPV types

• Some retroviruses

9. Q: What viruses are transmitted through droplets or aerosols?

A:

• Influenza

• Rhinovirus

• Measles

• Vaccinia virus

• SARS-CoV-2

10. Q: Which viruses can be transmitted through sexual contact?

A:

• Human papillomavirus (HPV)

• Hepatitis B virus (HBV)

• HSV type II (HSV-2)

11. Q: Which virus is associated with hand-to-face transmission in the lecture?

A: Epstein-Barr virus (EBV). Hand-to-face transmission can also occur with influenza and SARS-CoV-2.

12. Q: Which viruses can be transmitted through blood?

A:

• HIV

• HBV

• HCV

• Ebola virus

13. Q: What is fecal-oral transmission? Give an example.

A: Transmission occurs when virus-containing fecal material is swallowed, often through contaminated food or hands. Example: hepatitis A virus.

14. Q: What are fomites? Give examples of viruses transmitted this way.

A: Fomites are contaminated objects or surfaces that can transmit infectious agents. Examples include:

• Norwalk virus

• Rhinovirus

• Coronaviruses

15. Q: What is zoonotic transmission? Give examples.

A: Transmission of an infectious agent from animals to humans.

Examples:

• Rabies virus: animal bite

• Hantavirus: inhalation of particles associated with infected deer mice

• Avian influenza: associated with birds

16. Q: What is vector transmission? Give examples.

A: Transmission through an arthropod, such as a mosquito, fly, or tick.

Examples:

• Dengue virus

• West Nile virus

• La Crosse virus

• Yellow fever virus

17. Q: What does localized viral infection mean? Give examples.

A: The virus remains near its entry site, which is also where it replicates.

Examples:

• Rhinovirus: upper respiratory tract

• SARS-CoV-2: respiratory tract

• Rotavirus: intestinal epithelium

• Papillomavirus: epidermis

18. Q: What are the two major routes viruses use to spread to the central nervous system (CNS)?

A:

• Hematogenous spread: through the bloodstream.

• Neuronal spread: through peripheral nerves.

19. Q: Which viruses can spread to the CNS through neuronal pathways?

A:

• Enteroviruses, such as poliovirus: GI tract to CNS

• VZV and measles: respiratory tract to skin and peripheral nervous system

• HSV: urogenital tract to peripheral and central nervous systems

• Rabies: muscle/connective tissue to CNS

20. Q: Which viruses spread hematogenously, and where can they spread?

A:

• HBV and HCV: through the bloodstream to the liver.

• HIV: from the urogenital tract to lymph nodes.

21. Q: What are the major innate immune defenses against viral infections?

A:

• Type I interferons (IFN)

• Tumor necrosis factor-alpha (TNF-α)

• Natural killer (NK) cells

• Macrophages

22. Q: What triggers the innate immune response against viruses?

A: Recognition of viral molecular patterns by the innate immune system.

23. Q: Which immune cells are especially important in adaptive immunity against viruses?

A:

• Cytotoxic T cells

• Helper T cells

24. Q: What do cytotoxic T cells do during viral infections?

A: They destroy virus-infected cells or help eliminate the infection from those cells.

25. Q: What do helper T cells do during viral infections?

A: They help coordinate the immune response by promoting antibody production and cytotoxic T-cell activity.

26. Q: How do antibodies and complement help defend against viruses?

A: They limit viral spread and help prevent reinfection.

27. Q: How do viral mutations help viruses evade the immune system?

A: Low-fidelity viral polymerases produce mutations. Some mutations allow viruses to change their antigens and escape immune recognition or become resistant to antivirals.

28. Q: What is selection of an escape mutant?

A: When immune pressure or antiviral treatment eliminates susceptible viruses, resistant or immune-escaping variants can become dominant.

29. Q: How does latency help viruses evade the immune system?

A: Latent viruses express few or no viral antigens, making them harder for the immune system to recognize and eliminate.

30. Q: How does downregulation of MHC class I help viruses evade immunity?

A: It reduces antigen processing and presentation, making it harder for infected cells to alert cytotoxic T cells. Examples: CMV, HSV, and HIV.

31. Q: What are other mechanisms viruses use to evade the immune system?

A:

• Infection of immune-privileged sites, such as the brain.

• HSV glycoproteins interfere with complement activation.

• HIV destroys CD4 helper T cells.

• HIV increases Fas ligand expression on the cell surface.

32. Q: What are the major laboratory methods used to diagnose viral infections?

A:

• Viral culture using cell lines or eggs

• Antigen and antibody detection, including ELISA and Western blot

• PCR

• Histology/immunohistochemistry

• Electron microscopy

33. Q: What are cytopathic effects (CPEs)? Give examples.

A: Visible changes in host cells caused by viral infection.

Examples:

• Cell necrosis

• Inclusion bodies

• Giant cells

• Cytoplasmic vacuolation

34. Q: What are plaques in viral culture, and how are they different from bacterial colonies?

A: Plaques are clear areas where viruses have destroyed cells. Bacterial colonies represent bacterial growth, while viral plaques represent areas of cell damage or death.

35. Q: What are common features of acute respiratory viral infections?

A: They commonly spread through droplets, aerosols, or saliva and usually remain localized to the respiratory tract. Some become systemic.

Examples of respiratory viruses:

• Adenovirus

• Rhinovirus

• Influenza

• Coxsackievirus

• Respiratory syncytial virus (RSV)

36. Q: Which viruses can cause common cold, pharyngitis, croup, and bronchiolitis?

A:

• Common cold: rhinovirus; some coronaviruses.

• Pharyngitis: adenovirus and Coxsackievirus.

• Croup/laryngitis: mainly parainfluenza.

• Bronchiolitis: RSV and parainfluenza.

37. Q: What must gastrointestinal viruses be able to withstand to cause infection?

A: They must resist stomach acid and bile to reach the intestines.

38. Q: What antibody is important in protecting the gastrointestinal tract against viral infections?

A: Secretory IgA (sIgA), which helps neutralize viruses at mucosal surfaces.

39. Q: Which viruses commonly cause gastrointestinal infections in infants and children versus adults?

A:

Infants and children	Adults
Rotavirus	Enterovirus
Norovirus	Coronavirus
Poliovirus	Adenovirus
Hepatitis A
Calicivirus

40. Q: How can viruses enter the skin, and what is an example of each route?

A:

• Abrasions: poxviruses, HPV, HSV.

• Animal bites: rabies virus.

• Needle punctures: HBV and HIV.

41. Q: What are the different types of skin lesions associated with viral infections?

A:

• Macules

• Papules

• Vesicles

• Pustules

Viral infections can also cause ulceration and scabbing.

42. Q: How do viruses reach the CNS, and what happens during CNS infection?

A: Viruses enter through the bloodstream or spread along peripheral nerves. CNS infection can cause inflammation and tissue damage, with microglia participating in the immune response.

43. Q: Which viruses are associated with subacute sclerosing panencephalitis and progressive multifocal leukoencephalopathy?

A:

• Subacute sclerosing panencephalitis (SSPE): measles virus.

• Progressive multifocal leukoencephalopathy (PML): JC polyomavirus.

44. Q: Which viruses are the primary causes of congenital viral infections according to the lecture?

A:

• Cytomegalovirus (CMV)

• Rubella virus

Other viruses include HSV, VZV, HBV, measles, mumps, HIV, parvovirus, and some enteroviruses.

45. Q: Why are congenital viral infections especially concerning early in pregnancy?

A: The earlier the infection occurs during pregnancy, the more extensive the potential fetal damage.

46. Q: What are possible outcomes of congenital viral infections?

A:

• Fetal death

• Premature birth

• Intrauterine growth restriction

• Persistent postnatal infection

• Congenital heart defects

• Cataracts

• Deafness

• Microcephaly

• Limb hypoplasia

47. Q: What does TORCH stand for?

A:

• T: Toxoplasma

• O: Other diseases

• R: Rubella virus

• C: Cytomegalovirus

• H: Herpes simplex virus

48. Q: How does host age affect viral disease severity? Give examples from the lecture.

A: Age can influence susceptibility and disease severity.

Examples:

• Rubella: especially serious during gestation.

• Rotavirus: especially serious in infants.

• St. Louis encephalitis and SARS-CoV-2: more serious in elderly individuals.

49. Q: Why is selective toxicity difficult to achieve with antiviral drugs?

A: Viruses use the host cell's machinery to replicate, so blocking viral replication without damaging host cells is difficult.

50. Q: Why is timing important when giving antiviral drugs?

A: Viral replication often occurs during the incubation period, before symptoms appear. Treatment may be less effective once symptoms develop.

51. Q: What are nucleoside and nucleotide analogs, and how do they work?

A: They resemble normal DNA/RNA building blocks but can prevent further chain extension, inhibiting viral genome replication.

52. Q: How does acyclovir inhibit viral replication?

A: Acyclovir resembles guanosine but lacks the normal 3′-OH needed for chain extension. Once incorporated into viral DNA, it prevents further DNA-chain elongation.

53. Q: What do reverse transcriptase inhibitors block, and which viruses are they used against?

A: They block reverse transcriptase, an enzyme that converts RNA into DNA.

The lecture mentions their use against:

• HIV

• HBV

• HTLV

54. Q: What do protease inhibitors block, and which viruses are they used against?

A: They block viral proteases, which are needed to process viral proteins.

Examples from the lecture:

• HIV

• HCV

55. Q: What do integrase inhibitors and fusion inhibitors do?

A:

• Integrase inhibitors: Block integration of viral DNA into the host genome.

• Fusion inhibitors: Prevent the viral envelope from fusing with the host cell membrane.

56. Q: What do amantadine and oseltamivir (Tamiflu) inhibit?

A:

• Amantadine: Inhibits viral uncoating; historically used for influenza, but resistance has limited its usefulness.

• Oseltamivir (Tamiflu): Inhibits influenza neuraminidase, reducing viral release from infected cells.

57. Q: What are prions, and how are they different from viruses?

A: Prions are infectious proteins that contain no nucleic acid. Viruses contain DNA or RNA surrounded by a protein capsid and may also have an envelope.

58. Q: What disease do prions cause, and what are its major characteristics?

A: Spongiform encephalopathy, a rare, progressive neurodegenerative disorder characterized by a long incubation period and eventual severe disease.

59. Q: How does a normal prion protein become an abnormal prion, and how does the abnormal protein spread?

A:

• Normal prion protein (PrP) is primarily folded into alpha-helical structures.

• Abnormal prion protein (PrPSc) contains increased beta-sheet structure.

• The abnormal protein can cause normal prion proteins to misfold into the abnormal form.

• This creates a self-propagating process.

60. Q: What are the major prion diseases, how can prions be transmitted, and why are they difficult to eliminate?

A:

Disease	Associated animal or host
Creutzfeldt-Jakob disease (CJD)	Humans
Kuru	Humans
Bovine spongiform encephalopathy (BSE)	Cattle; mad cow disease
Scrapie	Sheep
Chronic wasting disease (CWD)	Deer and elk
Mink encephalopathy	Mink

Transmission examples from the lecture:

• Contaminated animal-derived material.

• Contaminated surgical equipment.

• Corneal transplantation.

• Cadaver-derived growth hormone.

• Ritual exposure to infected tissue (historical Kuru transmission).

Why they are difficult to eliminate: Abnormal prion proteins are highly resistant to ordinary disinfectants and standard sterilization procedures. The lecture describes additional decontamination measures beyond standard autoclaving.

High-yield summary tables

Viral infection outcomes

Type	Viral activity	Host cell outcome	Examples
Acute	Rapid replication	Usually cell death	Influenza
Chronic	Ongoing replication	Cell death may occur later	HIV, HCV
Latent	Minimal/no expression	Genome persists; can reactivate	HSV, EBV, VZV

Viral immunity

Immune defense	Main function
Type I IFN	Innate antiviral response
TNF-α	Innate inflammatory response
NK cells	Help eliminate infected cells
Macrophages	Innate immune defense
Cytotoxic T cells	Destroy infected cells
Helper T cells	Promote antibody and cytotoxic T-cell responses
Antibodies + complement	Limit viral spread and reinfection

Antiviral drug mechanisms

Drug class	What it inhibits
Nucleoside/nucleotide analogs	Viral DNA/RNA chain extension
Reverse transcriptase inhibitors	RNA-to-DNA conversion
Protease inhibitors	Viral protein processing
Integrase inhibitors	Integration of viral DNA
Fusion inhibitors	Viral-host membrane fusion
Amantadine	Viral uncoating
Oseltamivir	Influenza neuraminidase

Key prion facts

Normal prion	Abnormal prion
PrP	PrPSc
More alpha-helical structure	More beta-sheet structure
Normal protein	Misfolded infectious protein
Can be converted into abnormal form	Can induce misfolding of normal proteins