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Review Question - QID 217768

QID 217768 (Type "217768" in App Search)
A 31-year-old woman presents to her primary care physician with a 2-day history of a blister around her mouth. She says that she has recently been stressed and feels like she always gets blisters during stressful situations. She first experiences itching in the affected area and then notices redness and blister formation the next day. Her past medical history is significant only for anxiety for which she does not take any medications. Her temperature is 98.6°F (37°C), blood pressure is 113/76 mmHg, pulse is 91/min, and respirations are 13/min. Physical exam reveals the findings shown in Figure A but is otherwise unremarkable. Which of the following principles is the most likely cause of this patient's repeated symptoms?
  • A

Antigenic drift

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Antigenic shift

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Complementation

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Latency

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Recombination

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  • A

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This patient who presents with recurrent episodes of pruritic oral vesicles on an erythematous base most likely has oral herpes. This disease can present multiple times due to virus latency in the trigeminal ganglia.

Oral herpes is an infection of the oral mucous membrane typically by herpes simplex virus (HSV) type 1 but sometimes also by HSV type 2. Initial infection with HSV usually occurs in childhood and results in fever and other systemic symptoms. After this initial exposure, oral herpes enters a latent phase inside the trigeminal ganglia where virus genetic material has very little activity and thus evades detection by the immune system as no antigens that can be recognized are expressed. During times of stress, oral herpes can then reactivate from latency due to triggering of viral protein translation from latent genetic material, resulting in a prodrome of itching, tingling, or burning followed by grouped vesicles on an erythematous base. The diagnosis can be made clinically; however, viral culture or PCR can confirm the diagnosis in uncertain cases. Treatment includes acyclovir and valacyclovir.

Yu et al. studied the factors leading to reactivation of HSV from latency. They found that the interaction between regulatory T cells and CD8+ T cells is critical in mediating the balance between latency and reactivation. They recommend further research on these pathways.

Figure/Illustration A is a clinical photograph of the oral mucosa with herpes blisters (yellow circle). These lesions are classically described as grouped vesicles on an erythematous base.

Incorrect Answers:
Answer 1: Antigenic drift is a viral genetic principle where genetic material will undergo point mutations in surface proteins such that the same virus can partially evade immune detection. Seasonal flu epidemics are caused by antigenic drift as previously exposed patients can become reinfected.

Answer 2: Antigenic shift is a viral genetic principle where viruses with segmented genomes exchange segments and cause genetic reassortment. This is the process that results in flu pandemics where a novel cell surface protein completely evades the immune response and leads to severe illness in previously exposed individuals. Infectivity is high, since there is no underlying immunity to the novel strain in the population.

Answer 3: Complementation is a viral genetic principle where a virus with a functional protein helps a defective virus with a non-functional mutation replicate. This is the principle that underlies the superinfection of hepatitis D in patients who are already infected with hepatitis B.

Answer 5: Recombination is a viral genetic principle where 2 different viral strains infect the same host cell and interact during replication to generate progeny that have a combination of genes from both parent strains.

Bullet Summary:
Latency of herpesvirus in the trigeminal ganglion results in periodic reactivation of oral lesions in infected patients.

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