Patterns of Infection Flashcards
(24 cards)
Match the following terms to their definitions:
1) Viral pathogenesis
2) Acute infection
3) Persistent infection
A) pattern of infection whereby the viral infection is not cleared by the immune system (long-term infection). can be divided into multiple types (i.e. latent, asymptomatic, pathogenic). viral genomes may remain. no single mechanism!
B) adverse physiological consequences that occur as a result of viral infection of the host organism.
C) pattern of infection whereby virus particles produce rapidly & infection is resolved relatively quickly by the immune system (short-term infection).
Viral pathogenesis: adverse physiological consequences that occur as a result of viral infection of the host organism.
Acute infection: pattern of infection whereby virus particles produce rapidly & infection is resolved relatively quickly by the immune system (short-term infection).
Persistent infection: pattern of infection whereby the viral infection is not cleared by the immune system (long-term infection). can be divided into multiple types (i.e. latent, asymptomatic, pathogenic). viral genomes may remain. no single mechanism!
The pathogenesis that may follow a viral infection relies on _______ ______ in addition to its impact on infected cells.
Several parameters
*ex: what tissue do the cells reside? what is the overall fitness of the host? what is the age & immunological history of the host?
Match the following persistent patterns of infection to their definitions:
1) Persistent - Latent
2) Persistent - Asymptomatic
3) Persistent - Pathogenic
A) Virus production continues for the life of the host or in tissues where immune cells do not often patrol (symptoms may not be apparent)
B) Period of years separates primary infection and fatal appearance of symptoms; production of virus particles may be continuous or not detectable throughout life (HIV)
C) Periodic episodes of ACUTE INFECTIONS followed by QUIESCENT phase (little/no detection of viral particles); reactivation stimulated throughout host life (may result in virus particle production)
Persistent - Latent: Periodic episodes of ACUTE INFECTIONS followed by QUIESCENT phase (little/no detection of viral particles); reactivation stimulated throughout host life (may result in virus particle production)
Persistent - Asymptomatic: Virus production continues for the life of the host or in tissues where immune cells do not often patrol (symptoms may not be apparent)
Persistent - Pathogenic: Period of years separates primary infection and fatal appearance of symptoms; production of virus particles may be continuous or not detectable throughout life (HIV)
Virus infections exhibit incubation periods. What is an incubation period?
The period of time before SYMPTOMS of disease appear following initial infection. During this period, viral genomes may be replicated & innate immune responses initiate production of cytokines (i.e. type I interferons)
(T/F) Incubation periods for all viruses are the same!
False!
Incubation periods can vary significantly depending on the virus that establishes the infection.
Match the order of a typical acute viral infection:
1) Step 1
2) Step 2
3) Step 3
4) Step 4
5) Step 5
6) Step 6
A) Establishment of infection after a certain threshold (specific to virus + host)
B) Clearing of virus and memory (B/T cells) produced during the adaptive response stored, providing long-lasting protection to subsequent infections
C) Entry of virus
D) Adaptive response, which causes a decline in the # of viral particles
E) Innate defences start to kick in
F) Induction of adaptive response after infection reaches the threshold
Step 1: Entry of virus
Step 2: Innate defences start to kick in
Step 3: Establishment of infection after a certain threshold (specific to virus + host)
Step 4: Induction of adaptive response after infection reaches the threshold
Step 5: Adaptive response, which causes a decline in the # of viral particles
Step 6: Clearing of virus and memory (B/T cells) produced during the adaptive response stored, providing long-lasting protection to subsequent infections
What is common to persistent infections even though there is no single mechanism responsible for establishing them?
Persistent infection may be likely when viral cytopathic effects are minimized and host defences are suppressed.
A feature of establishing persistent infection is the REDUCTION OF HOST DEFENSES. Modulation of the adaptive immune response may perpetuate a persistent infection!
How can viruses modulate the adaptive immune response and create a persistent infection?
Viral gene products may block presentation of viral peptides within MHC I complexes at several steps within the pathway (i.e. lowering expression of MHC I genes, blocking production of proteasome-derived viral peptides, interfering with MHC I biogenesis & transport to cell surface)
This type of immune modulation may prevent or delay elimination of virus by cytotoxic T cells!
What do rhinovirus, rotavirus, and influenza virus have in common?
They cause acute infections!
Match the following viruses to their associated disease:
1) Rhinovirus
2) Rotavirus
3) Influenza virus
A) respiratory tract infection
B) common cold
C) gastroenteritis
Rhinovirus: common cold
Rotavirus: gastroenteritis
Influenza virus: respiratory tract infection
Which virus causes persistent LATENT infection?
Herpes simplex virus!
Which one of the statements is true regarding latent infections?
1) Viral gene products that promote virus reproduction are continuously synthesized in large quantities.
2) Cells that contain the viral genome may be poorly recognized by the immune system.
3) The viral genome does not always persists intact within the infected cell.
2!
1) Viral gene products that promote virus reproduction MAY NOT BE continuously synthesized (or synthesized in SMALL quantities).
3) The viral genome PERSISTS INTACT within the infected cell to ensure productive infection may be initiated at a later time. Ensures that virus progeny may be transmitted to new hosts.
How is the latent genome maintained in non-dividing cells vs dividing cells?
Is there any other mechanism?
Non-dividing cells: NON-REPLICATING CHROMOSOME
Dividing cells: AUTONOMOUS REPLICATING CHROMOSOME
It can also be INTEGRATED into host CHROMOSOME.
What causes reactivation of latent infections?
Reactivation may be STOCHASTIC or may follow a certain type of insult (i.e. STRESS, TRAUMA).
The mechanism depends on specific virus.
Human herpesvirus is an _______ virus with a ________ genome.
enveloped; dsDNA
Briefly answer the following questions regarding the herpes virus:
1) What are two kinds and how are they transmitted?
2) Where does it cause infection?
3) What is the associated disease?
1) HHV-1: saliva & HHV-2: sexual contact & maternal-neonatal
2) Primary site of infection in epithelial mucosal cells. Latency established in sensory ganglia.
3) Skin vesicles or mucosal ulcers
Match the following steps of a herpes simplex virus (HSV-1) infection cycle:
1) Step 1
2) Step 2
3) Step 3
4) Step 4
5) Step 5
A) Factors such as hormonal changes, environmental stress may REACTIVATE the virus
B) Immune responses are re-activated and CONTROLS LOCAL infection by KILLING epithelial cells, producing a NEW SORE.
C) HSV-1 infects EPITHELIAL CELLS and spreads to SENSORY NEURONS
D) Virus can then travel down the axons of the sensory neurons and RE-INFECTS the epithelial tissues
E) After immune response controls the epithelial infection, the virus persists in a LATENT STATE in the sensory neurons
Step 1: HSV-1 infects EPITHELIAL CELLS and spreads to SENSORY NEURONS
Step 2: After immune response controls the epithelial infection, the virus persists in a LATENT STATE in the sensory neurons
Step 3: Factors such as hormonal changes, environmental stress may REACTIVATE the virus
Step 4: Virus can then travel down the axons of the sensory neurons and RE-INFECTS the epithelial tissues
Step 5: Immune responses are re-activated and CONTROLS LOCAL infection by KILLING epithelial cells, producing a NEW SORE.
(T/F) HSV-1 can spread from epithelial cell to cell.
True!
Fill in the blanks regarding the establishment of latency of HSV-1:
Infection in epithelial cells at ________ surfaces.
Virus enters sensory neurons; _________ transported to the neuronal cell body via _________-based systems.
Viral DNA is released into the _______ _____ & _________.
This DNA persists in the neuronal cell nucleus; _________ ______ _____ is expressed.
Mucosal
Nucleocapsids; microtubule
Neuronal nucleus; circularizes
Latency Associated Transcript (LAT)
Fill in the blanks regarding the REACTIVATION of HSV-1:
Viral gene _____ is initiated, and newly formed capsids are transported to the _______ ______.
Infectious virus is released from the _____ and infects ________ cells, resulting in recurrent infection and virus _________.
Expression; axonal termini
Axon; epithelial; shedding
What are Latency Associated Transcripts (LATs)?
These transcripts are expressed during latent expression when lytic genes are blocked.
They contribute to gene silencing to maintain latent state!
Match the steps of varicella-zoster virus infection:
1) Step 1
2) Step 2
3) Step 3
4) Step 4
5) Step 5
6) Step 6
A) Virus particles may then be released into the bloodstream again, causing a SECONDARY VIREMIA
B) Virus produced in skin infect SENSORY NERVE & spread to SENSORY GANGLIA where a LATENT infection is established
C) Infection of CONJUNCTIVA or MUCOSA of upper RESPIRATORY TRACT, followed by spread to LYMPH NODES
D) Reactivation may occur later in life; virus infects the skin which leads to HERPES ZOSTER (shingles)
E) Entry into bloodstream, causing PRIMARY VIREMIA (virus in the blood), which then target other organs such as LIVER & SPLEEN
F) Dissemination of virus to skin; leads to characteristic VESICULAR RASH (chicken pox)
Step 1: Infection of CONJUNCTIVA or MUCOSA of upper RESPIRATORY TRACT, followed by spread to LYMPH NODES
Step 2: Entry into bloodstream, causing PRIMARY VIREMIA (virus in the blood), which then target other organs such as LIVER & SPLEEN
Step 3: Virus particles may then be released into the bloodstream again, causing a SECONDARY VIREMIA
Step 4: Dissemination of virus to skin; leads to characteristic VESICULAR RASH (chicken pox)
Step 5: Virus produced in skin infect SENSORY NERVE & spread to SENSORY GANGLIA where a LATENT infection is established
Step 6: Reactivation may occur later in life; virus infects the skin which leads to HERPES ZOSTER (shingles)
(T/F) The introduction of the varicella vaccine in 1995 reduced the number of varicella cases substantially.
True!
Hospitalizations and deaths in children declined by >95% once 2-dose programme was established.
Clinical signs of viral disease (fever, aches, tissue damage, nausea) largely stem from the _____ ________ response to infection.
This damage is referred to as __________ (may be the price to pay by the hos to eliminate infection!)
Host’s immune
Immunopathology
