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Year : 2020  |  Volume : 3  |  Issue : 2  |  Page : 368-369

Authors' reply to Kulkarni et al. and Wiwanitkit

Department of Medical Oncology, Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India

Date of Submission27-Mar-2020
Date of Decision28-Mar-2020
Date of Acceptance29-Mar-2020
Date of Web Publication19-Jun-2020

Correspondence Address:
Kumar Prabhash
Department of Medical Oncology, Tata Memorial Hospital, Parel, Mumbai - 400 012, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/CRST.CRST_97_20

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How to cite this article:
Agrawal AK, Rajendra A, Noronha V, Joshi A, Patil V, Menon N, Talreja V, Prabhash K. Authors' reply to Kulkarni et al. and Wiwanitkit. Cancer Res Stat Treat 2020;3:368-9

How to cite this URL:
Agrawal AK, Rajendra A, Noronha V, Joshi A, Patil V, Menon N, Talreja V, Prabhash K. Authors' reply to Kulkarni et al. and Wiwanitkit. Cancer Res Stat Treat [serial online] 2020 [cited 2020 Sep 18];3:368-9. Available from: http://www.crstonline.com/text.asp?2020/3/2/368/287283

We thank Kulkarni et al.[1] and Wiwanitkit [2] for their interesting comments on our article, “Cytomegalovirus infection in solid malignancies,” and the accompanying editorial.[3],[4] Kulkarni et al. have discussed several important aspects of cytomegalovirus (CMV) infection, such as the latency of CMV infection because of the active cellular immunity of the host and its reactivation due to various possible reasons. CMV, a β-herpesvirus, replicates slowly but can affect multiple cell types within a single host. During latency, the myeloid progenitor cells act as virus reservoirs, however, other cell types may also contribute.[5] Experiments on mice engrafted with human CD34+ hematopoietic precursor cells have shown the reactivation of CMV from latency in response to the granulocyte-colony-stimulating factor.[6]

The antileukemic effect of CMV infection, which is most pronounced in patients with acute myeloid leukemia, is termed as the virus-versus-leukemia effect. This is probably mediated by the memory natural killer cells and γ/δ T-cells, which proliferate in response to CMV infection.[7]

Wiwanitkit concurs that like patients with hematological malignancies, patients with solid tumors should also be tested for CMV reactivation, as they too are immunocompromised. Moreover, he has discussed another important aspect – the carcinogenic property of CMV.[2] Literature suggests a high prevalence of CMV in various tumor types including rhabdomyosarcoma, hepatocellular cancers, brain tumors, prostate cancer, and cancers of the breast, colon, and salivary glands.[8] In vitro animal studies have shown that the CMV genome can lead to transformation of cells.[9] This suggests a possible role of CMV as a carcinogen. However, the potential role of CMV in tumorigenesis has also been criticized, as other in vitro experiments have shown that most CMV strains are unable to transform human cells.[8] Therefore, it is still unclear whether CMV is an oncogenic virus, and this remains a subject of research to guide us further.

Overall, CMV poses many challenges and opportunities in terms of managing the morbidity related to its infection, understanding the immunological mechanisms underlying its latency-reactivation pathway, and deciphering its possible role in oncogenesis and the human immune system.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kulkarni AP, Bhosale SJ. Reactivation of Cytomegalovirus: Another thing to worry about? Cancer Res Stat Treat 2020;3:367-8.  Back to cited text no. 1
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Wiwanitkit V. Cytomegalovirus infection and solid tumor. Cancer Res Stat Treat 2020;3:366.  Back to cited text no. 2
  [Full text]  
Agrawal AK, Rajendra A, Noronha V, Joshi A, Patil VM, Menon N, Talreja V, Prabhash K. Cytomegalovirus infection in solid malignancies. Cancer Res Stat Treat 2020;3:19.  Back to cited text no. 3
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Bansal N, Ghafur KA. Cytomegalovirus reactivation in solid tumors: Are we missing the bus (bug)? Cancer Res Stat Treat 2020;3:76.  Back to cited text no. 4
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Goodrum F. Human cytomegalovirus latency: Approaching the Gordian Knot. Annu Rev Virol 2016;3:333-57.  Back to cited text no. 5
Crawford LB, Streblow DN, Hakki M, Nelson JA, Caposio P. Humanized mouse models of human cytomegalovirus infection. Curr Opin Virol 2015;13:86-92.  Back to cited text no. 6
Elmaagacli AH, Koldehoff M. Cytomegalovirus replication reduces the relapse incidence in patients with acute myeloid leukemia. Blood 2016;128:456-9.  Back to cited text no. 7
Nauclér CS, Geisler J, Vetvik K. The emerging role of human cytomegalovirus infection in human carcinogenesis: A review of current evidence and potential therapeutic implications. Oncotarget 2019;10:4333-47.  Back to cited text no. 8
Nelson JA, Fleckenstein B, Jahn G, Galloway DA, McDougall JK. Structure of the transforming region of human cytomegalovirus AD169. J Virol 1984;49:109-15.  Back to cited text no. 9


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