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Year : 2020  |  Volume : 3  |  Issue : 2  |  Page : 367-368

Reactivation of Cytomegalovirus: Another thing to worry about?

Division of Critical Care Medicine, Department of Anaesthesiology, Critical Care and Pain, Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India

Date of Submission26-Mar-2020
Date of Decision26-Mar-2020
Date of Acceptance27-Mar-2020
Date of Web Publication19-Jun-2020

Correspondence Address:
Atul Prabhakar Kulkarni
Division of Critical Care Medicine, Department of Anaesthesiology, Critical Care and Pain, Tata Memorial Hospital, Homi Bhabha National Institute, Dr. Ernest Borges Road, Parel, Mumbai - 400 012, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/CRST.CRST_95_20

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How to cite this article:
Kulkarni AP, Bhosale SJ. Reactivation of Cytomegalovirus: Another thing to worry about?. Cancer Res Stat Treat 2020;3:367-8

How to cite this URL:
Kulkarni AP, Bhosale SJ. Reactivation of Cytomegalovirus: Another thing to worry about?. Cancer Res Stat Treat [serial online] 2020 [cited 2021 Apr 18];3:367-8. Available from: https://www.crstonline.com/text.asp?2020/3/2/367/287281

We read with great interest the article by Agrawal et al. and the accompanying editorial.[1],[2] In a retrospective single-center study on patients with solid tumors, they found that the Cytomegalovirus (CMV) coexisted with other infections in 10 out of 17 patients. Interestingly, the median time to CMV reactivation was only 1.5 months. The mortality in this cohort was 42%, but it increased to 70% when the patients required intensive care unit (ICU) admission. These data emphasize the need for a high index of suspicion and early treatment, as large studies in this group are scarce.

In a recent editorial, Reddehase makes some very important points. He suggests that CMV has coexisted with species-specific hosts forever. The CMV adapts to the host environment by acquiring species-specific genes that control the host immune response by modulating the inherent, characteristic adaptive defense mechanisms. At the same time, the hosts have developed counter strategies to defend themselves. Thus, CMV remains latent without causing infection because of the active cellular immunity, but it is still capable of reactivation when conditions become favorable.[3]

In the current series, there were various features that made the reactivation of CMV possible. Eight (47%) patients were neutropenic and were given granulocyte colony-stimulating factors (GCSFs). Smith et al. found that the use of GCSF, which caused mobilization of hematopoietic cells from the bone marrow in humanized mice, led to reactivation of latent CMV infection, which spread to involve various organs.[4] There were other plausible reasons for immunosuppression in the current cohort, such as preexisting HIV-positive status, diabetes mellitus, and therapy with prednisolone in 3, 3, and 2 patients, respectively.[1]

In the present study, only those patients who showed clinical manifestations of CMV or were nonresponders to other antimicrobials as a part of the infection workup underwent testing for CMV DNA using reverse transcription polymerase chain reaction.[1] This is another aspect to be mindful of, particularly because of the scarcity of resources in developing countries.

The effect of CMV reactivation in immunocompetent patients with sepsis is unclear. Heininger et al. observed an increase in the duration of mechanical ventilation and the length of hospital stay as a result of CMV reactivation.[5] However, previous studies have shown an increase in mortality in patients with sepsis with CMV reactivation.[6] In the study by Limaye et al., however, the average number of copies was many more than that in the study by Heininger et al. Further quantitative studies are therefore needed in immunocompetent patients with sepsis.

Finally, can CMV reactivation be beneficial in any way? Litjens et al. suggest two possible benefits: protection against relapse of acute myeloid leukemia in patients who have undergone allogeneic hematopoietic stem cell transplantation and a possible increase in acceptance after allograft liver transplantation. Only time will tell.[7]

  References Top

Agrawal AK, Rajendra A, Noronha V, Joshi A, Patil VM, Menon N, et al. Cytomegalovirus infection in solid malignancies. Cancer Res Stat Treat 2020;3:19-24.  Back to cited text no. 1
  [Full text]  
Bansal N, Ghafur KA. Cytomegalovirus reactivation in solid tumors: Are we missing the bus (bug)? Cancer Res Stat Treat 2020;3:76-7.  Back to cited text no. 2
  [Full text]  
Reddehase MJ. 'Checks and balances' in cytomegalovirus-host cohabitation. Med Microbiol Immunol 2019;208:259-61.  Back to cited text no. 3
Smith MS, Goldman DC, Bailey AS, Pfaffle DL, Kreklywich CN, Spencer DB, et al. Granulocyte-colony stimulating factor reactivates human cytomegalovirus in a latently infected humanized mouse model. Cell Host Microbe 2010;8:284-91.  Back to cited text no. 4
Heininger A, Haeberle H, Fischer I, Beck R, Riessen R, Rohde F, et al. Cytomegalovirus reactivation and associated outcome of critically ill patients with severe sepsis. Crit Care 2011;15:R77.  Back to cited text no. 5
Limaye AP, Kirby KA, Rubenfeld GD, Leisenring WM, Bulger EM, Neff MJ, et al. Cytomegalovirus reactivation in critically ill immunocompetent patients. JAMA 2008;300:413-22.  Back to cited text no. 6
Litjens NH, van der Wagen L, Kuball J, Kwekkeboom J. Potential Beneficial effects of cytomegalovirus infection after transplantation. Front Immunol 2018;9:389.  Back to cited text no. 7

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1 Authorsę reply to Kulkarni et al. and Wiwanitkit
AmitKumar Agrawal,Akhil Rajendra,Vanita Noronha,Amit Joshi,Vijay Patil,Nandini Menon,Vikas Talreja,Kumar Prabhash
Cancer Research, Statistics, and Treatment. 2020; 3(2): 368
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