Block 9 Micro Viral Pathogenesis
Pathogens are microorganisms that cause disease and we get to understand how they do so by taking a pathogenesis course. Pathogens of all classes must have mechanisms for entering their host and for evading immediate destruction by the host immune system. To see how much you understood from block 9 micro viral pathogenesis take up the quiz below.
- 1.
A 1-year-old toddler is admitted to the hospital in February following an abrupt onset of vomiting followed by watery diarrhea accompanied by low-grade fever. On admission, the child appears somnolent, has a fever of 38.8C (101.8F). His pulse is 130/min, respiratory rate 36/min, blood pressure 100/60 mmHg, and decreased skin turgor. Blood tests reveal an elevated white blood cell count (15,000/L) with 75% polymorphonuclear leukocytes. A stool sample is sent to the microbiology lab for analysis. Results reveal watery stools with no mucus, blood, leukocytes or parasites. A rapid antigen test is positive for a naked, segmented, dsRNA virus, so no stool culture is required. The diarrhea suffered by this child can be partially attributed to a viral protein (rotavirus NSP4) that alters the permeability of intestinal epithelial cell tight junctions and inhibits the glucose-coupled Na+ transport of these same cells, thereby increasing osmotic gap. What best describes this virulence mechanism?
- A.
Alteration of viral replication or of the cell cycle
- B.
Alteration of host defense mechanisms
- C.
Facilitation of viral spread
- D.
Toxicity
Correct Answer
D. ToxicityExplanation
The virulence mechanism described in the question is toxicity. The viral protein NSP4 produced by the rotavirus alters the permeability of intestinal epithelial cell tight junctions and inhibits the glucose-coupled Na+ transport of these cells. This leads to an increase in the osmotic gap and ultimately causes the watery diarrhea experienced by the child. This mechanism is considered toxic as it directly affects the normal functioning of the intestinal cells and disrupts their ability to absorb water and electrolytes properly.Rate this question:
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- 2.
Virulence mechanisms play an important role in the pathogenesis of viral infections and these include mechanisms (1) that alter viral replication, (2) that alter host defense mechanisms, (3) that facilitate viral spread and (4) that are toxic to the host. Which of the following mechanisms would most likely be involved in viral spread in the human population?
- A.
Apoptosis
- B.
Autophagy
- C.
Virokines
- D.
Viroceptors
- E.
Antigenic drift
Correct Answer
E. Antigenic driftExplanation
Antigenic drift would most likely be involved in viral spread in the human population. Antigenic drift refers to the gradual accumulation of small genetic changes or mutations in the viral genome over time. These changes can lead to the production of slightly different viral strains that may not be recognized by the immune system, allowing the virus to evade immune responses and spread more easily within the population.Rate this question:
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- 3.
Which of the following assertions is true?
- A.
Terminally differentiated cells such as neurons are permissive to viral infection.
- B.
Viral dissemination is invariably hindered by inflammation
- C.
Polarized cells are non-permissive to viral infection
- D.
Syncytia formation is a means of systemic dissemination
- E.
Low pH is always detrimental to viruses
Correct Answer
A. Terminally differentiated cells such as neurons are permissive to viral infection.Explanation
Terminally differentiated cells, such as neurons, are permissive to viral infection. This means that these cells are susceptible to being infected by viruses. Unlike other cell types that may have defense mechanisms to prevent viral entry, terminally differentiated cells do not have these protective mechanisms, making them more vulnerable to viral infection. This is why viruses can successfully infect and replicate within neurons and other terminally differentiated cells.Rate this question:
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- 4.
Which of the following statements is false?
- A.
The successful infection of a host requires a minimum number of inoculating viruses
- B.
The successful infection of a host requires terminally differentiated cells
- C.
The successful infection of a host requires that the host cell is susceptible to the infection.
- D.
The successful infection of a host requires that the host possesses inefficient local viral defenses at the time of infection
- E.
The successful infection of a host requires that the host cells are accessible to the viruses.
Correct Answer
B. The successful infection of a host requires terminally differentiated cellsExplanation
The successful infection of a host does not necessarily require terminally differentiated cells. Many viruses can infect a wide range of cell types, including both undifferentiated and differentiated cells. Therefore, the statement that the successful infection of a host requires terminally differentiated cells is false.Rate this question:
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- 5.
Virulence mechanisms play an important role in the pathogenesis of viral infections and these include mechanisms (1) that alter viral replication, (2) that alter host defense mechanisms, (3) that facilitate viral spread and (4) that are toxic to the host. Which of the following mechanisms would favour viral replication?
- A.
Apoptosis
- B.
Virally-encoded proteins that increase cell cycling
- C.
Virokines
- D.
Viroceptors
- E.
The tandem action of the double-stranded RNA (dsRNA) binding proteins 2’,5’-oligo(A) synthetase and RNase L
Correct Answer
B. Virally-encoded proteins that increase cell cyclingExplanation
Virally-encoded proteins that increase cell cycling would favor viral replication because they promote the cell cycle progression, leading to increased cell division and proliferation. This provides more host cells for the virus to infect and replicate within, enhancing viral replication.Rate this question:
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- 6.
Virulence mechanisms play an important role in the pathogenesis of viral infections and some of these factors alter host defense mechanisms. One such factor is adenovirus E3-gp19K which inhibits MHC-I transport to the cell surface. Which host defense mechanism is affected by E3-gp19K?
- A.
B cell-mediated antigen presentation to naïve CD4+ cells
- B.
CD4+-mediated B cell activation
- C.
Dendritic cell-mediated antigen presentation to naïve CD4+ cells
- D.
Somatic cell-mediated antigen presentation to activated CD8+ cells
- E.
CD4+-mediated CD8+ cell activation
Correct Answer
D. Somatic cell-mediated antigen presentation to activated CD8+ cellsExplanation
Adenovirus E3-gp19K inhibits MHC-I transport to the cell surface. MHC-I molecules are responsible for presenting antigens to CD8+ cells, which are cytotoxic T cells. Therefore, the host defense mechanism affected by E3-gp19K is somatic cell-mediated antigen presentation to activated CD8+ cells. This inhibition hinders the ability of CD8+ cells to recognize and eliminate virus-infected cells, allowing the virus to evade the immune response.Rate this question:
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- 7.
All but one of these statements are true. Which one?
- A.
Modes of viral transmission often dictate the tissues that will be infected and infected tissues often determine modes of transmission
- B.
Modes of viral transmission seldom dictate the tissues that will be infected, but infected tissues often determine modes of transmission
- C.
Modes of viral transmission often dictate the tissues that will be infected, but infected tissues seldom determine modes of transmission
- D.
Modes of viral transmission seldom dictate the tissues that will be infected nor do infected tissues ever determine modes of transmission
- E.
Modes of viral transmission randomly dictate the tissues that will be infected and infected tissues have random modes of transmission
Correct Answer
E. Modes of viral transmission randomly dictate the tissues that will be infected and infected tissues have random modes of transmissionExplanation
The correct answer is "Modes of viral transmission seldom dictate the tissues that will be infected, but infected tissues often determine modes of transmission." This statement suggests that viral transmission does not have a strong influence on which tissues will be infected, but once a tissue is infected, it can determine how the virus is transmitted. This implies that the choice of tissues infected is not random, but the mode of transmission can vary depending on the infected tissue.Rate this question:
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- 8.
What is the most direct mode of tissue damage resulting from virus infections?
- A.
Cell destruction by NK cells
- B.
Cell destruction by CTLs
- C.
Cytolysis due to viral release
- D.
Cell destruction by macrophages
- E.
Cell destruction by neutrophils
Correct Answer
C. Cytolysis due to viral releaseExplanation
Cytolysis due to viral release refers to the direct destruction of cells caused by the release of viruses from infected cells. When viruses replicate inside host cells, they eventually burst and release new virus particles, leading to the destruction of the infected cells. This mode of tissue damage is considered the most direct because it occurs as a result of the virus itself and not due to the immune response.Rate this question:
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- 9.
Besides cell lysis, what is(are) the most common mode(s) of tissue damage resulting from viral infections?
- A.
Cell destruction by NK cells
- B.
Cell destruction by CTLs
- C.
Cell destruction by mast cells
- D.
Cell destruction by macrophages
- E.
Cell destruction by neutrophils
Correct Answer(s)
A. Cell destruction by NK cells
B. Cell destruction by CTLsExplanation
During viral infections, besides cell lysis, the most common modes of tissue damage are cell destruction by NK cells and cell destruction by CTLs. NK cells and CTLs are part of the immune system and play a crucial role in eliminating virus-infected cells. They recognize and kill these cells, leading to tissue damage. Mast cells, macrophages, and neutrophils are also involved in the immune response to viral infections but are not the primary cells responsible for cell destruction.Rate this question:
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- 10.
All but one of these statements are true. Which one?
- A.
Retroviral gp41 (TM protein) increases HIV virulence
- B.
Some viruses incorporate host-cell surface proteins
- C.
Virokines are antiviral host molecules
- D.
Pustules can be a way to spread an infection from one host to another.
- E.
RNA-dependent RNA polymerase is prone to error and is a cause for increased virulence.
Correct Answer
C. Virokines are antiviral host moleculesExplanation
The given answer is correct because it states that "Virokines are antiviral host molecules." This means that virokines are molecules produced by the host that have antiviral properties. The other statements in the question are either unrelated to the concept of virokines or are not true. Retroviral gp41 (TM protein) actually increases HIV virulence, some viruses do incorporate host-cell surface proteins, pustules can be a way to spread infection, and RNA-dependent RNA polymerase is prone to error but it is not specifically mentioned as a cause for increased virulence.Rate this question:
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- 11.
A 37-year-old female presents to her gynecologist for a routine exam. Pertinent history reveals that it has been 5 years since her last exam, she is a smoker (half pack per day), had her first intercourse at age 15, has had 9 sexual partners over her lifetime and is on oral contraceptives. Gynecological exam is normal, except for lesions on the cervix seen by colposcopy. A Papanicolaou smear (Pap smear) from a lesion reveals the presence of high-grade squamous intraepithelial lesions (HSILs). In situ hybridization performed on a cervical biopsy from the same patient shows that cervical epithelial cells in the lesions contain L1 DNA belonging to the Human papillomavirus type 16. Inhibition of cyclin-dependent kinase inhibitors by HPV-16 protein E7 contribute significantly to the cellular transformation process. What best describes this pathophysiological mechanism?
- A.
Alteration of viral replication or of the cell cycle
- B.
Alteration of host defense mechanisms
- C.
Facilitation of viral spread
- D.
Toxicity
Correct Answer
A. Alteration of viral replication or of the cell cycleExplanation
The presence of high-grade squamous intraepithelial lesions (HSILs) on the cervix, along with the detection of Human papillomavirus type 16 (HPV-16) in the cervical epithelial cells, indicates that the patient has an HPV infection. The HPV-16 protein E7 inhibits cyclin-dependent kinase inhibitors, which leads to an alteration in the cell cycle. This alteration in the cell cycle allows the HPV virus to replicate and persist within the cervical epithelial cells, leading to the development of HSILs. Therefore, the pathophysiological mechanism in this case is the alteration of viral replication or of the cell cycle.Rate this question:
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- 12.
Virulence mechanisms play an important role in the pathogenesis of viral infections. Such mechanisms are involved in (1) the alteration of viral replication, (2) the alteration of host defense mechanisms, (3) the facilitation of viral spread and (4) host toxicity. Which of the following is an example of a virulence mechanism that contributes to disease due to the production of a toxin?
- A.
Human cytomegalovirus viroceptor expression
- B.
Rotavirus NSP4 protein expression
- C.
Influenzavirus HA (hemagglutinin) protein expression
- D.
Human papillomavirus DNA polymerase expression
Correct Answer
B. Rotavirus NSP4 protein expressionExplanation
Rotavirus NSP4 protein expression is an example of a virulence mechanism that contributes to disease due to the production of a toxin. This suggests that the NSP4 protein produced by rotavirus plays a role in the pathogenesis of the viral infection by causing toxicity in the host.Rate this question:
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- 13.
Human herpesvirus 1 (HSV-1) gE-gI is a virally-encoded Fc-gamma receptor (crystallizable fragment-gamma receptor, or vFc-R) that localizes in both the virus envelope and the cell membrane of HSV-1-infected cells, thereby protecting the virus from clearance by the immune system. Which of the following immune responses is(are) most likely to be affected by gE-gI?
- A.
Major histocompatibility complex class I (MHC class I)-antigen presentation
- B.
Alternative pathway of complement activation
- C.
Antibody-dependent cell cytotoxicity (ADCC)
- D.
CD8+ cytotoxic T lymphocyte (CTL) cytotoxicity
Correct Answer
C. Antibody-dependent cell cytotoxicity (ADCC)Explanation
The gE-gI protein of HSV-1 is known to be a virally-encoded Fc-gamma receptor that is present in both the virus envelope and the cell membrane of infected cells. This protein plays a role in protecting the virus from clearance by the immune system. Antibody-dependent cell cytotoxicity (ADCC) is a mechanism by which immune cells, such as natural killer cells, recognize and kill virus-infected cells that are bound by antibodies. Since gE-gI is a receptor for antibodies, it is likely to affect ADCC, as it may interfere with the recognition and killing of infected cells by immune cells.Rate this question:
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- 14.
16.1) A previously healthy 52-year-old man presents in the early stages of cirrhosis. It turns out that his cirrhosis is the result of an infection with the hepatitis C virus he acquired three decades ago. Contributing factors for the development of silent disease are (1) the capacity of the virus to suppress IFN- secretion by interfering with signaling downstream of TLR-3 and RIG-1, as well as (2) suppressing STAT-1 activation. How do these factors benefit the virus?
- A.
Suppression of ADCC
- B.
Suppression of NK cell-mediated cell cytotoxicity
- C.
Suppression of CTL-mediated cell cytotoxicity
- D.
Suppression of classical pathway of complement activation
- E.
Suppression of Pkr- and 2’,5’ OAS/RNase L-mediated apoptosis
Correct Answer
E. Suppression of Pkr- and 2’,5’ OAS/RNase L-mediated apoptosisExplanation
The factors mentioned, suppression of Pkr- and 2’,5’ OAS/RNase L-mediated apoptosis, benefit the hepatitis C virus by preventing the infected cells from undergoing programmed cell death. This allows the virus to persist and replicate within the cells without being eliminated by the immune system. Apoptosis is a natural defense mechanism of the body to remove infected cells, but the virus interferes with this process, enabling its survival and continued infection.Rate this question:
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- 15.
16.2) What best describes this virulence mechanism?
- A.
Alteration of viral replication or of the cell cycle
- B.
Alteration of host defense mechanisms
- C.
Facilitation of viral spread
- D.
Toxicity
Correct Answer
B. Alteration of host defense mechanismsExplanation
This virulence mechanism involves altering the host's defense mechanisms. This means that the virus is able to manipulate or impair the immune response of the host, making it easier for the virus to establish infection and evade elimination by the immune system. By weakening the host's defense mechanisms, the virus can effectively increase its ability to replicate and spread within the host's body.Rate this question:
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- 16.
17.1) Orf virus (Poxviridae), the etiologic agent for a rare occupational zoonosis called contagious pustular dermatitis, encodes a homologue of IL-10. Which of the following functions would mostly be affected by this homologue?
- A.
Alternate pathway of complement activation
- B.
Lectin pathway of complement activation
- C.
Classical pathway of complement activation
- D.
T helper 1 response
- E.
T helper 17 response
Correct Answer
D. T helper 1 responseExplanation
The homologue of IL-10 encoded by the Orf virus would mostly affect the T helper 1 response. IL-10 is a cytokine that plays a role in regulating the immune response. It is known to suppress the activity of T helper 1 cells, which are involved in cellular immunity and the production of pro-inflammatory cytokines. Therefore, the presence of the IL-10 homologue in the Orf virus would likely dampen the T helper 1 response, potentially allowing the virus to evade the immune system and establish infection.Rate this question:
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- 17.
17.2) What term best describes this molecule?
- A.
Viroceptor
- B.
Virokine
- C.
Cytokine
- D.
Virosubducer
- E.
Cytoceptor
Correct Answer
B. VirokineExplanation
Virokine is the best term to describe this molecule. The term "viro" suggests that it is related to viruses, and "kine" indicates that it is a signaling molecule. Therefore, virokine refers to a molecule produced by viruses that can modulate the immune response of the host. This term accurately describes the function and origin of the molecule.Rate this question:
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Current Version
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Mar 21, 2023Quiz Edited by
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Jun 07, 2012Quiz Created by
Chachelly
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