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Winter course I > Viro > Flashcards

Viro Flashcards

1
Q

What is the genetic/p-distance?

A

The proportion of nucleotidesat which 2 sequences differ

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2
Q

What is the R0 value?

A

The reproduction number at t=0, where an R0 of 2 means 1 person infects 2 people.

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3
Q

What is the critical value of R0?

A

1, meaning that an R0 of under 1 means unsufficient transmissibility to continue spreading in the population, since 1 person infects less than 1 person on average.

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4
Q

What is PrEP?

A

Pre-exposure prophylaxis, usually taken by people that are at higher risk of contracting HIV, if available to them.

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5
Q

On the host side, what determines transmissibility of an STD via sexual intercourse? (3)

A

Tropism, viral load and transmission fitness

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6
Q

What can influence determines viral load on the host side in the context of an STD? (2)

A

Treatment, stage of infection

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7
Q

On the interface side, what determines transmissibility of an STD via sexual intercourse? (2)

A

Condom, type of sexual intercourse

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8
Q

On the recipient side, what determines transmissibility of an STD via sexual intercourse? (5)

A

STD status, tropism, PrEP, PEP, gender

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9
Q

How can removing foreskin help protect against contracting HIV?

A

It removes the langerhans cells which can take u the virus and help facilitate dissemination

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10
Q

What are the 3 stages of an HIV infection?

A

Acute stage, chronic stage and AIDS

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11
Q

What is the average time from infection to death in HIV?

A

10 years

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12
Q

How long does the HIV acute stage take?

A

10-16 weeks

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13
Q

How many HIV patients report symptoms in the acute stage?

A

50%

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14
Q

What are the typical symptoms during acute HIV infection?

A

Flu-like (headache, fever, swollen lymph nodes, malaise, rash)

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15
Q

How long does the chronic HIV stage last?

A

Usually ~8 years

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16
Q

What are the typical symptoms during chronic HIV?

A

Frequently no symptoms, sometimes tiredness, swollen lymph nodes

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17
Q

What happens to the virus during chronic HIV?

A

10^9 produced every day, they destroy the immune system by infecting CD4 T cells

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18
Q

What happens during AIDS?

A

Opportunistic infections due to immunocompromised state. Sometimes accompanied by weight loss (wasting) and dementia.

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19
Q

When are people most infectious during HIV infection?

A

The acute stage, which is why U=U may not end the epidemic

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20
Q

How probable is HIV transmission during sexual intercourse?

A

Low, sexual exposure rarely leads to infection. It is a bit higher in MSM (but still low)

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21
Q

What is the most efficient route of transmission of HIV?

A

Blood transfusion

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22
Q

How many genomes are needed to establish an HIV infection?

A

At most 2

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23
Q

What is the Fiebig staging system?

A

A way of classifying early HIV infection into five sequential stages based on HIV test result patterns in newly diagnosed individuals

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24
Q

What is an example of how tests results can indicate which Fiebig stage a patient is in?

A

Viral RNA is detected but a western blot is negative against antibodies -> one of the earliest stages, since RNA is the first thing to come up

25
Q

How can the amount of viral genomes at the time of infection be established retrospectively?

A

Molecular clock analysis using genomes from early stage HIV patient. Very low genetic variation (p-distance) indicates a low number of viruses having been transmitted at t=0.

26
Q

What is the poisson distribution?

A

The numer of mutations per unit of time (ex: 0.05 mutations per day)

27
Q

Why does a chronic infection have such a diverse population of viruses?

A

High replication rate and no proofreading

28
Q

What are a quasi-species?

A

A group of mutant viruses that develops as a virus replicates within a host. As David calls it: a “cloud” of genetically different viruses

29
Q

Do all quasispecies have an equal chance of transmitting?

A

No, most of them are defective. Only the most fit will establish infection in a new host.

30
Q

Does HIV immediately disseminate throught the body?

A

No, it is initially a local infection until it is fully established after 2-5 days

31
Q

Why does PEP work?

A

Window of opportunity: It can stop the virus during the local stage before it disseminates out of the mucosa and establishes productive infection in the LN

32
Q

When were the first depictions of polio?

A

Ancient egypt

33
Q

When was polio first discovered?

A

1909

34
Q

What are the 5 main clinical outcomes of polio?

A

Asymptomatic
Non-paralytic (typical viral symptoms)
Non-paralytic CNS disease (meningitis)
Papalytic poliomyelitis (accide flaccid paralysis)
Bulbar paralytic polio myelitis (involvement of the brain stem)

35
Q

How many people recover from paralytic disease? How many are permanently paralyzed? How many fatalities?

A

10%, 80%, 10%

36
Q

What is post-polio syndrome?

A

Like long covid. Happend 15-60 years after paralytic or non-paralytic disease in 20-75% of patients

37
Q

What were the first vaccines developed?

A

Salk inactivated (1955)
Sabin live-attenuated vaccine (1961-62)

38
Q

When was polio first propagated, and what did that lead to?

A

Identification of 3 serotypes that can cause paralytic disease, and generation of vaccines

39
Q

What is the advantage of Salk (inactivated poliovirus vaccine)?

A

Almost 100% seroconversion, no severe side effects

40
Q

What are the disadvantages of Salk?

A

Cold chain
Expensive
Needles required (kids)
Low intestinal immunity

41
Q

What are the advantages of Sabin?

A

Cheap
Intestinal immuntiy
Passine immunization (transmissible)
No cold chain
Oral drops

42
Q

What are disadvantages of Sabin?

A

Can acquire mutations
Vaccin-associated paralytic poliomyelitis
Circulation of VCPV

43
Q

What is the Global Polio Eradication Initiative?

A

Initiated in 1988, with the goal to complete eradication and containment of all wild type and vaccine-related polioviruses, such that no child ever again suffers paralytic poliomyelitis

44
Q

What has the Global Polio Eradication Initiative achieved sofar?

A

Incidence decreased by 99%, and WPV type 2 and 3 have been eradicated

45
Q

What is the bulk of the still circulating polio?

A

Vaccine-derived, mostly in African countries (due to cold chain problems)

46
Q

What is the biggest problem with full wild-type eradicatioin currently?

A

Afghanistan government (Taliban)

47
Q

What is used to address cVDPV?

A

nOPV-2, which is more genetically stable and reversion is really rare in comparison

48
Q

What is better than nOPV-2?

A

Inactivated Polio Vaccine (IPV)

49
Q

What is being increased to continue in the eradication movement?

A

Surveillance and Outbreak response capacity

50
Q

When did acute flaccid paralysis caused by EV-D68 start popping up more?

A

2014

51
Q

Why did EV-D68 suddenly start causing AFP?

A

We don’t know. It is not clade-specific and only popped up every 2 years until 2018

52
Q

What is the pathogenesis of EV-D68?

A

We know that it is more like a rhino, preferring 33 degrees and being acid sensitive unlike other enteroviruses

53
Q

What is the pathogenesis of neurological disease in EV-D68?

A

We only know it can target motor neurons in the spinal cord

54
Q

What is the proposed pathogenesis of Poliovirus?

A

Mucosa
LN
Viremia
Skeletal muscles
Motor end plate
Via motor neurons to the spine and then brain

55
Q

What is the proposed pathogenesis of EV-D68?

A

Respiratory tract (upper and/or lower)
Viremia
LN
Maybe skeletal muscles
Motor neurons
Brain?

56
Q

How can EV-D68 go systemic?

A

It can cause viremia, it can replicate in lymphoid tissue and in lymphoid cells (B cells).
It is also sometimes detected in stool samples, suggesting it can infect intestinal cells (in vitro)

57
Q

How can EV-D68 invade the brain?

A

We don’t know. We do know that iPSC-derived motor neurons are susceptible.

58
Q

What can be used to prevent acute flaccid myelitis?

A

Antibodies

59
Q
A

Winter course I (3 decks)

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