Table of Contents  
LETTER TO THE EDITOR
Year : 2016  |  Volume : 9  |  Issue : 2  |  Page : 277-278  

Lessons from "the Berlin patient"


1 Department of Radio-Diagnosis, Dr. D. Y. Patil Medical College, Pune, Maharashtra, India
2 Department of Physiotherapy, Dr. D. Y. Patil Medical College, Pune, Maharashtra, India

Date of Web Publication1-Mar-2016

Correspondence Address:
Dhaval Thakkar
403, Alaknanda, Neelkanth Valley, Ghatkopar (East), Mumbai - 400 077, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.177697

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How to cite this article:
Thakkar D, Kharat A, Jantre M, Singh A, Pagare V. Lessons from "the Berlin patient". Med J DY Patil Univ 2016;9:277-8

How to cite this URL:
Thakkar D, Kharat A, Jantre M, Singh A, Pagare V. Lessons from "the Berlin patient". Med J DY Patil Univ [serial online] 2016 [cited 2024 Mar 29];9:277-8. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2016/9/2/277/177697

Sir,

Human immunodeficiency virus-acquired immune deficiency syndrome (HIV-AIDS), caused by infection with the HIV, is the leading infectious cause of morbidity and mortality worldwide. The WHO reports 35 million people living with HIV-AIDS worldwide in 2013, with 1.5 million people dying of AIDS-related illness worldwide in 2013. Furthermore, a total of 78 million have been infected since the beginning of the epidemic. [1] Although the introduction of highly active anti-retroviral therapy (HAART) has harnessed the epidemic to some extent and transformed HIV-AIDS into a chronic disease state, HIV still remains a major global health problem today.

The acquisition of infection with HIV-1 involves the binding of the virus to the CD4 receptor on immune cells to enter them; this requires the concomitant interaction of the virus with a co-receptor on the target cell, which can be either CCR5 or CXCR4. Individuals who are homozygous for a 32-basepair deletion in the CCR5 allele (known as the delta32 deletion) have been found to be naturally resistant to acquiring HIV-1 infection.

In 2009, Hütter et al. from Berlin reported a successful transplantation of allogeneic stem-cells from a donor homozygous for the CCR5 delta32 allele to a patient with HIV. The indication for transplantation was acute myeloid leukemia. [2] In this patient, now famous as "the Berlin patient," transplantation resulted in complete chimerism, and the patient's peripheral-blood monocytes changed from a heterozygous to a homozygous genotype with regards to the CCR5 delta32 allele. HAART was discontinued from the day of transplantation. Although discontinuation of HAART typically leads to a rapid rebound of HIV load within weeks, HIV could not be detected in this patient 20 months after HAART was discontinued. For as long as the viral load continues to be undetectable, re-initiation of HAART will not be required in this case. Therefore, the Berlin patient is considered the only person in the world to have been successful "cured" of HIV infection.

Prior to this case, attempts to control HIV-1 infection by means of allogeneic stem-cell transplantation did not take the donor's CCR5 delta32 into consideration and were not successful. [2] We believe that the Berlin patient reiterates the central role of the CCR5 receptor during HIV-1 infection, and warrants further investigation into the development of CCR5-targeted treatment options, as well as allogenic stem-cell transplants, in the management of HIV-AIDS.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Global Health Observatory (GHO) Data. Switzerland: World Health Organisation and Map Production: Health statistics and Information systems (HSI) World Health Organization -Available from: http://www.who.int/gho/hiv/en/. [Last cited on 2014 Mar 22].  Back to cited text no. 1
    
2.
Hütter G, Nowak D, Mossner M, Ganepola S, Müssig A, Allers K, et al. Long-term control of HIV by CCR5 Delta32/Delta32 stem-cell transplantation. N Engl J Med 2009;360:692-8.  Back to cited text no. 2
    




 

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