B3 measles Flashcards

1
Q

What happens in an acute symptomatic infection?

A

→ Infection of a small number of cells, followed by multiple cycles of viral replication.

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2
Q

How does an acute infection spread?

A

It can stay local or spread systemically.

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3
Q

What are the outcomes of an acute symptomatic infection?

A

Clearance by the immune response and recovery, or progression to chronic/latent infection or death.

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4
Q

What is the typical duration of an acute symptomatic infection?

A

Days to weeks.

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5
Q

How contagious is measles?

A

One of the most contagious diseases.

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6
Q

What is the mortality rate of measles in developed countries?

A

→ 0.1%.

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7
Q

What is the mortality rate of measles in developing countries?

A

→ 5-10%.

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8
Q

How are paramyxoviruses transmitted?

A

Readily via the respiratory route.

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9
Q

What are the two patterns of infection caused by paramyxoviruses?

A
  1. Localised respiratory infections (e.g., RSV, hMPV). 2. Systemic infections (e.g., measles, mumps).
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10
Q

Why are paramyxoviruses dangerous for infants?

A

Localised respiratory infections are trivial in adults but can be severe in infants and children.

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11
Q

How is measles transmitted?

A

Aerosol droplets.

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12
Q

Where does measles initially replicate?

A

Upper respiratory tract epithelium.

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13
Q

What happens in primary viraemia?

A

Virus is mainly associated with lymphocytes and macrophages, with little free virus in the blood.

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14
Q

Where does measles replicate after primary viraemia?

A

Lymphoid tissues (spleen, lymph nodes, appendix, tonsils).

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15
Q

What happens in secondary viraemia?

A

Virus spreads to organs such as skin, conjunctiva, liver, kidney, lungs, and gut.

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16
Q

What causes the characteristic measles rash?

A

Immune response to virus-infected endothelial cells.

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17
Q

What are the main symptoms of measles?

A

Fever, cough, runny nose (coryza), conjunctivitis, maculopapular rash.

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18
Q

What are Koplik’s spots?

A

White spots inside the mouth, a hallmark of measles.

19
Q

What is giant cell pneumonia?

A

Severe pneumonia caused by syncytia formation, often fatal in immunocompromised patients.

20
Q

How does measles suppress the immune system?

A

Infects and depletes memory B and T cells, causing “immune amnesia” and increased risk of secondary infections.

21
Q

What bacterial infections are common after measles?

A

Otitis media (ear infection) and pneumonia (~15% of cases).

22
Q

What is the leading cause of measles-related deaths?

A

Pneumonia (60% of deaths).

23
Q

What is measles encephalitis?

A

Inflammation of the brain, occurring in 1 in 1000 cases, often causing neural damage.

24
Q

What is SSPE?

A

A rare, fatal, slow-progressing CNS disease occurring years after measles infection.

25
Q

Who is at highest risk of SSPE?

A

Males and those infected with measles under 2 years old.

26
Q

What causes SSPE?

A

Persistent defective (non-infectious) measles virus in the brain, triggering a hyperimmune response.

27
Q

What type of genome does measles have?

A

Negative-sense single-stranded RNA (-ve ssRNA).

28
Q

What proteins are important for measles virus entry?

A

H protein (docking) and F protein (fusion).

29
Q

What cellular receptors does measles target?

A

CD46/CD150 on lymphocytes and epithelial cells.

30
Q

What is the function of RdRp in measles?

A

Transcribes the genome into mRNA and replicates it into a full-length positive-sense copy.

31
Q

How does measles virus assemble and release?

A

F & H proteins move to the cell membrane, M protein associates with RNP, leading to viral release.

32
Q

What is syncytia formation, and why is it important?

A

Measles virus induces fusion of infected cells, forming multinucleated giant cells.

33
Q

What is more important for clearing measles: T cells or antibodies?

A

→ T cells.

34
Q

What causes the symptoms of measles?

A

Immune response rather than direct viral damage (e.g., cytokines cause fever, T cells attack infected endothelial cells causing rash).

35
Q

Why is the absence of a rash a bad sign in measles?

A

→ Indicates poor T cell response and poor prognosis.

36
Q

What is required for lifelong immunity to measles?

A

A strong antibody response (IgG) prevents reinfection.

37
Q

Why is measles vaccine effective?

A

Only one serotype, live attenuated vaccine, induces a strong immune response.

38
Q

What does the MMR vaccine protect against?

A

Measles, mumps, and rubella.

39
Q

hy are two doses of measles vaccine given?

A

First dose may be neutralised by maternal antibodies; second dose ensures full immunity.

40
Q

Why is high vaccine uptake essential?

A

To achieve herd immunity and break the chain of transmission.

41
Q

What are examples of localised acute infections caused by paramyxoviruses?

A

Respiratory syncytial virus (RSV) and human metapneumovirus (hMPV).

42
Q

Why does measles have little free virus in the blood during primary viraemia?

A

The virus is mostly associated with immune cells like lymphocytes and macrophages.

43
Q

What does “gradient of transcripts” mean in measles virus transcription?

A

RdRp transcribes genes in a sequential manner, leading to higher levels of 5’ genes and lower levels of 3’ genes.