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Viral Pathogenesis > Acute Infections > Flashcards

Acute Infections Flashcards

1
Q

Influenza A incubation period

A

1-5 days

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2
Q

Influenza A symptoms

A

Headache, chills, dry cough, fever. The fever declines and will be gone within a week. The cough and weakness may persist up to 2 weeks

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3
Q

Complications of influenza

A
  1. Viral pneumonia can lead to bacterial pneumonia
  2. Cardiac complications
  3. Myositis- muscle pain and weakness
    Pre-existing conditions can pre-dispose someone to complications
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4
Q

Antigenic variation

A

Antigenic drift- consists of small changes (or mutations) in the genes of influenza viruses that can lead to changes in the surface proteins of the virus, HA (hemagglutinin) and NA (neuraminidase). When a flu virus has become antigenically different (or “antigenically drifted”), this generally means that the virus’ antigenic properties are different enough that the body’s immune system (i.e., a person’s existing antibodies) will have a harder time recognizing and fighting against the virus.

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5
Q

Measles virus

A

A negative strand RNA virus in the Paramyxoviridae family. It is one of the most contagious viruses that is transmitted by respiratory droplets. Primary infections confer life-long immunity

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6
Q

Measles symptoms

A

The main symptoms are fever and rash

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7
Q

Progression of measles virus infection

A

Measles virus infects the immune cells of the respiratory tract. 2-3 days after replication in the lung, measles virus spreads to regional lymphoid tissues (primary viremia due to basement membrane decimation) followed by a systemic infection. Following further viral replication in regional and distal reticuloendothelial sites, a second viremia occurs 5 to 7 days after initial infection. Multiple organs, including the skin, may be affected. During this phase, infected lymphocytes and dendritic cells migrate into the subepithelial cell layer and transmit measles to epithelial cells in the lungs using the Nectin-4 receptor. Following amplification in the epithelia, the virus is released into the respiratory tract via apical spread. Respiratory shedding results

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8
Q

Timeline of measles virus infection (5)

A
  1. Primary viremia- early infection- the virus enters the body and infects the lymph nodes
  2. Secondary viremia- blood vessels carry virus-laden cells throughout the body
  3. Early symptoms- coughing, sneezing, and fevers emerge after viral loads peak. Koplik spots, fever, and malaise begin
  4. Rash- red bumps spread across the skin. Shedding continues and antibodies are produced
  5. Recovery- memory immune cells are depleted
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9
Q

Typical measles symptoms (7)

A
  1. Fever
  2. Dry cough
  3. Runny nose
  4. Sore throat
  5. Conjunctivitis
  6. Koplik’s spots- white spots on the inside of the cheek
  7. Rash
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10
Q

Measles complications (7)

A
  1. Ear infection
  2. Pneumonia
  3. Encephalitis: Subacute Sclerosing Panencephalitis (SSPE), degenerative neurological disease
  4. Bronchitis, Laryngitis
  5. Pregnancy problems- preterm labor, maternal death
  6. Immunosuppression: secondary infections may be life-threatening
  7. Immune Amnesia
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11
Q

Measles prevention

A

The measles vaccine was licensed in 1962-63 and combined into the MMR vaccine in 1971. Wakefield’s falsified study caused decreased vaccination in the UK. Anti-vaccine philosophies often contribute to outbreaks. In 2000, endemic transmission stopped due to vaccination

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12
Q

Impact of measles prior to MMR vaccination

A

There were 3-4 million infections per year, 48,000 hospitalizations, and 400-500 deaths per year

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13
Q

Poliovirus

A

A positive stranded RNA virus. It is well-adapted, meaning that 90% of infections are asymptomatic. Transmitted through the fecal-oral route, and the virus is able to withstand harsh gastrointestinal conditions. The virus replicates in the gut mucosa and sheds in feces, although it is eventually cleared in 99% of cases. In 1% of cases, the virus gets into the bloodstream and can enter the spinal cord or directly into brain tissue, crossing the blood brain barrier. Humans are the only known reservoir

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14
Q

Poliomyelitis pathology

A

Infected neurons exhibit a pyramidal shape. The virus destroys the neurons. Because there are fewer motor neurons, the remaining neurons sprout new fibers and grow bigger. This promotes recovery of the use of your muscles, but it also may stress the nerve cell body to nourish the additional fibers, leading to cervical and lumbar enlargement

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15
Q

Progression of polio

A

In most patients, infection is asymptomatic, and the virus is cleared within a week. In 1% of cases, there are severe outcomes such as paralysis. Symptoms before paralysis include fever, fatigue, vomiting, neck stiffness, headache, and limb pain. Paralytic symptoms- loss of reflexes, severe muscle aches or spasms, and flaccid paralysis, often worse on one side of the body. The onset of paralytic symptoms may be sudden

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16
Q

Post-polio syndrome

A

A post-polio syndrome that may develop over 30 years after polio infection. It is caused by polio damaging the neurons. Symptoms include fatigue, muscle and joint weakness and pain, muscle atrophy, and breathing or swallowing problems. Loss of neurons due to old age adds to the overall loss of neurons

17
Q

Polio prevention

A

Inactivated polio vaccine (Salk, 1955) and oral polio vaccine (Sabin, 1957)

18
Q

Influenza polybasic cleavage site

A

Multiple basic amino acids in the hemagglutinin (HA) cleavage site. This cleavage is a post-translational modification that allows the protein to mature. Low-pathogenic influenza A virus contains only a single type of amino acid (arginine) at the hemagglutinin cleavage site. However, these low-pathogenic viruses can be transformed into highly pathogenic viruses because of the acquisition of multiple basic amino acids at the hemagglutinin cleavage site. Variation in the amino acids introduce genetic variability, and more proteases can recognize and cleave the protein

19
Q

Antigenic shift

A

An abrupt, major change in a flu A virus, resulting in new HA and/or new HA and NA proteins in flu viruses that infect humans. Antigenic shift can result in a new flu A subtype infecting people for the first time

20
Q

Antigenic drift

A

Drift consists of small changes (or mutations) in the genes of influenza viruses that can lead to changes in the surface proteins of the virus, HA (hemagglutinin) and NA (neuraminidase). These changes occur continually as the virus replicates. The small genetic changes that occur in influenza viruses over time usually produce viruses that are closely related to one another and have similar antigenic properties

21
Q

Norovirus

A

A positive strand RNA virus that is part of the Caliciviridae family. It is responsible for more than 50% of gastroenteritis cases. Cases are most prevalent in the winter (November-April). It is highly contagious- 18 viral particles can cause illness. This virus results in 400 thousands ER visits and 800 deaths per year

22
Q

Norovirus pathogenesis

A

Commensal bacteria are required for Norovirus infection. Norovirus may interact with bacteria in the gut to enhance infection and replication. The virus infects Tuft cells, dendritic cells, B cells, and macrophages

23
Q

Norovirus symptoms

A

Diarrhea, vomiting, nausea, stomach pain, (molecular basis is unknown). Patients may be asymptomatic but contagious in 30% of cases

24
Q

Norovirus symptom duration

A

It takes 12-48 hours after exposure to develop symptoms, and symptoms may last up to 3 days

25
Q

Norovirus transmission

A

Spreads by contaminated food (fecal-oral)

26
Q

Norovirus gut pathology

A

Causes blunting of the villi (they are shorter)

27
Q

Acute infections

A

Mostly inapparent infection. Short course of infection, but may cause a severe course of disease. May cause rapid production of a large number of viruses. These infections are often cleared within a few days or weeks, predominantly by innate immunity and CTLs. Examples- influenza, SARS, rhinovirus. Asymptomatic acute infections pose greater challenges

28
Q

Serological surveys of acute infections

A

IgM antibodies are the main immunoglobulin species involved in the primary immune response, being produced early in the course of an infection. The secondary antibody response is characterized in its first few days by the production of small amounts of IgM antibody and larger amounts of IgG antibody, with some IgA and IgE

29
Q

Influenza A

A

Wild aquatic birds are natural hosts, although the virus primarily infects humans, poultry, and pigs. This strain is the most virulent and causes seasonal epidemics and pandemics. Can undergo reassortment

30
Q

Reassortment

A

Reassortment is the process by which influenza viruses swap gene segments. This genetic exchange is possible due to the segmented nature of the viral genome and occurs when two differing influenza viruses co-infect a cell. Plays a role in the evolution of the virus

31
Q

Influenza B

A

This strain predominantly infects humans and seals, and is less virulent than influenza A. Causes seasonal epidemics

32
Q

Influenza C

A

The least common strain, causes inapparent infections. Antigenic variation facilitates repeated acute infection. This strain has structural plasticity.

33
Q

Transmission routes of influenza (3)

A
  1. Droplets- coughing, sneezing, or talking
  2. Direct contact with an infected person
  3. Indirect contact through surfaces
34
Q

Tryptase

A

Restricts the IAV infection to the respiratory tract

35
Q

Transmembrane protease serine 2 (TMPRSS2)

A

Cleaves during entry via endosome

36
Q

Furin

A

Cleaves during assembly at the polybasic site (H5N1 caused multi-tissue tropism)

37
Q

Interventions for influenza

A
  1. Vaccines: Inactivated or LAIV
  2. Tamiflu- NA inhibitor, taken orally.
  3. Rapivab- NA inhibitor, intravenous.
  4. Relenza- NA inhibitor.
  5. Xofluza approved in 2018- Japan and USA)
38
Q

Xofluza

A

Targets the cap-dependent endonuclease activity of PA. It is single dose and reduces the duration of symptoms. Concern- prone to selection of resistant mutants

39
Q

Neuraminidase (NA) inhibitors

A

NA inhibitors inhibit the NA protein present on both influenza A and B, blocking the influenza virus from fusing with the host cell membrane. NA binds to sialic acid

Viral Pathogenesis (9 decks)

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