|LETTER TO EDITOR
|Year : 2020 | Volume
| Issue : 2 | Page : 368-369
Authors' reply to Kulkarni et al. and Wiwanitkit
Amit Kumar Agrawal, Akhil Rajendra, Vanita Noronha, Amit Joshi, Vijay Patil, Nandini Menon, Vikas Talreja, Kumar Prabhash
Department of Medical Oncology, Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India
|Date of Submission||27-Mar-2020|
|Date of Decision||28-Mar-2020|
|Date of Acceptance||29-Mar-2020|
|Date of Web Publication||19-Jun-2020|
Department of Medical Oncology, Tata Memorial Hospital, Parel, Mumbai - 400 012, Maharashtra
Source of Support: None, Conflict of Interest: None
|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. and Wiwanitkit  for their interesting comments on our article, “Cytomegalovirus infection in solid malignancies,” and the accompanying editorial., 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. 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.
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.
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. 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. In vitro animal studies have shown that the CMV genome can lead to transformation of cells. 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. 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.
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