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Acyclovir-resistant herpes simplex virus causing pneumonia after marrow transplantation
P Ljungman1, M N Ellis, R C Hackman
1Program in Infectious Diseases, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
Abstract:
Three marrow transplant patients developed pneumonia due to acyclovir-resistant thymidine-kinase-deficient herpes simplex virus (HSV) type 1. In all three, pneumonia was evident at autopsy by both standard and immunohistology, and virus was recovered from culture of lung tissue. Two patients also had other pulmonary infections at death; one had only HSV pneumonia. All had received prophylaxis and repeated treatment courses with acyclovir, and all initially had acyclovir-sensitive virus. The acyclovir-resistant HSV strains were sensitive to foscarnet, and in at least one case to vidarabine, but as expected were resistant to ganciclovir. These cases represent potentially severe visceral infection in which acyclovir-resistant virus strains were primary or important copathogens. Although acyclovir-resistant HSV is generally considered less virulent, these cases illustrate the potential importance of infection due to acyclovir-resistant HSV in severely immunocompromised patients. They also highlight the need to test HSV strains for antiviral sensitivity and to consider alternative therapies to acyclovir in appropriate clinical situations.
Insights
Acyclovir-resistant herpes simplex virus (HSV) caused severe pneumonia in three immunocompromised patients. Alternative antivirals like foscarnet are crucial when HSV develops resistance to acyclovir.
Area of Science:
- Virology
- Immunology
- Oncology
Background:
- Hematopoietic stem cell transplantation (HSCT) patients are highly susceptible to opportunistic infections.
- Herpes simplex virus (HSV) infections are common in immunocompromised individuals, typically managed with acyclovir.
Observation:
- Three HSCT recipients developed fatal pneumonia attributed to thymidine kinase-deficient, acyclovir-resistant HSV type 1.
- Autopsy revealed HSV pneumonia in all three cases, with virus isolated from lung tissue.
- Two patients had concurrent pulmonary infections, while one had HSV pneumonia as the sole identified cause of death.
Findings:
- The acyclovir-resistant HSV strains remained sensitive to foscarnet and vidarabine but not ganciclovir.
- These resistant strains acted as primary or significant co-pathogens in severe visceral disease.
- This challenges the notion that acyclovir-resistant HSV is always less virulent.
Implications:
- Highlights the critical need for routine antiviral sensitivity testing in immunocompromised patients with suspected HSV infections.
- Underscores the importance of considering alternative antiviral therapies, such as foscarnet, for acyclovir-resistant HSV.
- Emphasizes the potential severity of acyclovir-resistant HSV in severely immunocompromised populations, necessitating vigilant monitoring and tailored treatment strategies.