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Year : 2001  |  Volume : 55  |  Issue : 2  |  Page : 73-78

Seroprevalence of cytomegalovirus infection in Mauritian volunteer blood donors

Department of Biological Sciences, Faculty of Science, University of , Reduit, Mauritius

Correspondence Address:
A Pultoo
Department of Biological Sciences, Faculty of Science, University of , Reduit
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Source of Support: None, Conflict of Interest: None

PMID: 11482160

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How to cite this article:
Pultoo A, Meetoo G, Pyndiah M N, Khittoo G. Seroprevalence of cytomegalovirus infection in Mauritian volunteer blood donors. Indian J Med Sci 2001;55:73-8

How to cite this URL:
Pultoo A, Meetoo G, Pyndiah M N, Khittoo G. Seroprevalence of cytomegalovirus infection in Mauritian volunteer blood donors. Indian J Med Sci [serial online] 2001 [cited 2016 May 30];55:73-8. Available from:

Cytomegalovirus (CMV) is classified in the Herpesviridae family, which includes herpes simplex virus (HSV) type I and II that causes cold sores, Varicella­Zoster virus (VZV) causing chikenpox, and Epstein-Barr virus responsible for infectious mononucleosis. All these viruses have a relatively restricted host range and share a characteristic ability to remain dormant within the human body for a long period.[1] Cytomegalovirus is the largest member of the Herpesviridae family with a diameter of about 20 nm. The genome, which is surrounded by an icosahedral capsid of 162 capsomeres, is composed of approximately 240 kilobases of double stranded DNA with a capacity for encoding over 200 proteins. This nucleocapsid is itself enclosed by a spiked lipid envelope.[2]

The CMV infection is usually subclinical, but may cause serious morbidity and mortality in congenitally infected newborns and immunocompromised patients, most notably transplant recipients and HIV-infected persons.[1] Congenital infection often leads to diseases the most common of them being jaundice, hepatomegaly. Microcephaly, and mental retardation.[3] In immuno­compromised patients the clinical picture usually includes the development of interstitial pneumonitis, hepatitis, encephalitis, enteritis, trombocytopenia or leucopenia.[4]

There are several mechanisms of transmission of CMV infection, including congenitally acquired infection in neonates, sexual contacts, breast-feeding, saliva and blood transfusion.[1] Primary infection with CMV is invariably followed by life-long viral persistence in peripheral leucocytes.[5] Although CMV has a worldwide distribution, infection with CMV is more common in the developing countries and in areas of low socioeconomic conditions, which is predominantly due to closeness of contacts within these populations. In developing countries 80% of 3-year-old children and most adults have been shown to be infected with CMV. In contrast, research in England and the United States has shown only 40% to 60% of adults of middle to upper-class socioeconomic status are CMV seropositive, whereas 80% of adults of lower-class socioeconomic status have detectable antibody to CMV. [6]

CMV is known to be transmitted by blood transfusions. In 1960, a syndrome consisting of fever, atypical lymphocytosis, and splenomegaly was described in patients who had required large numbers of blood transfusion.[7] This 'post-perfusion' syndrome was later attributed, in most cases, to CMV infection acquired during blood transfusion.[8] CMV is believed to be transmitted in a latent noninfectious state by blood products and is reactivated after transfusion into the recipient.[9] This is in contrast with infections with other viruses such as hepatitis B and C and human immunodeficiency virus (HIV) are believed to result from transmission of infectious viruses present in blood of infected donors. A relatively small proportion of blood donors is infected with these viruses and reliable serologic techniques are available for screening and excluding these donors.[2]

The immunosuppressed population for whom CMV-­seronegative blood products are requested is increasing due to advances in medical care afforded to premature infants, the increasing use of transplantation procedures, immunosuppressive cancer therapies and spread of acquired immune deficiency syndrome (AIDS). This means that considerable stress is placed on blood banks to maintain adequate inventories of these products. In view of the increasing demand for CMV-free blood products, this study was performed to establish a panel of CMV seronegative blood donors since volunteer donors are expected to provide the major source of most blood transfusion requirements, and to determine the seroprevalence of CMV antibodies in Mauritian blood donors. The prevalence of CMV antibodies among the different sexes and age groups has also been investigated.

 ¤ Materials and methods Top

Study population: Between July and December 1999, 584 serum samples were tested from healthy volunteer blood donors. The donors were chosen independently of age or sex. There were 551 males and 33 females aged between 18 and 59 years (mean age 38 years).

Serology: The serum samples were examined by the complement fixation (CF) test. The CF test remains an adequate technique as it detects both IgG and IgM antibodies. Moreover, complement­fixing antibodies to CMV persist indefinity after a primary infections.[5] Complement fixation test is routinely used for epidemiological studies especially in patients with intact immunity as is the case in our study. Other tests including immunofluorescence (IF) based assays, radioimmunoassys (RIA), and enzyme-linked immunosorbent assays (ELISA), although more sensitive, do not substantially detect more seropositive individuals in a population.[2] A four-volume (0.025m1/ volume) CF test was performed in microplates using standard techniques for the estimation of CMV CF-antibody.[4] Commercial CMV CF-antigen, guinea-pig complement and anti­rabbit haemolysin were prepared by Virion diagnostics, Switzerland. Sheep erythrocytes were collected locally. The antigen was found to contain 1 unit (optimal peak dilution) at a dilution of 1/16 and the complement contained 1 unit (HD50) at a dilution of 1/50. These dilutions were calculated by chessboard titrations against a CMV-positive human serum. All sera were screened at a dilution of 1:5 for the presence or absence of CMV complement-fixing antibodies. Before testing specimens were inactivated for 30 minutes at 56°C. Two units of antigen and 2 units of complement were added to the specimens, and incubated overnight at 4°C, followed by addition of 2% sensitized sheep erythrocytes. The detection of specific antibodies was taken to indicate infection with CMV.

 ¤ Results Top

The prevalence of CMV antibodies was 93.5% (546 in 584) with 93.1 % in males and 100% in females [Table - 1] Only 38 sera gave CMV negative antibody tests. There was no statistically significant difference in seroprevalence between sexes (p>0.05). The prevalence of CMV antibodies in different age groups was also analyzed [Table - 1]. The prevalence seems to increase with age. However there was no statistically significant difference in CMV antibodies prevalence among the different age groups (p>0.05). Eighty percent of the population is already infected at the age of 18. The range varied from 80% in the 18-19 age group to 100% in the 45-59 age group.

 ¤ Discussion Top

The group of blood donors used in our study consisted of individuals belonging to different socioeconomic classes from several geographic regions of our country, living under various hygienic conditions. Hence, our data is probably a reflection of the current CMV seroprevalence in the Mauritian population. The seroprevalence of CMV antibodies in Mauritian volunteer healthy blood donors was very high (93%). Similar prevalence rates have been found in developing countries such as Thailand-93%.[10] Cameroon­-95%.[11] Jamaica-97%.[12] Tanzania-­98[13], and Nepal-100[14]. Our results also confirmed also confirmed that prevalence of CMV antibodies increases with age as reported by others[15] and higher prevalence of CMV antibodies in females than males.[9]

Complement-fixing antibodies to CMV appear to persist indefinitely after a primary infection, presumably because of the continued presence of the virus in the body in a latent phase. A study by Larsson et al.[5] showed that all seropositive donors harbour CMV in latently infected peripheral leucocytes. Since CMV is a cell­associated virus, the transmission may be due to the reactivation of the latent virus in white blood cells during blood transfusion. The high seroprevalence of CMV antibodies in the local blood donor population indicated that CMV-seronegative blood supply was very limited. Studies have shown that transfusion-transmitted CMV has been prevented using leucocyte depleted blood products.[1] Hence leucocyte-depleted blood by leucocyte filtration or counter-flow centrifugation techniques can be used as an alternative to CMV­seronegative blood in our local blood transfusion services. CMV infection after transfusion with CMV positive blood occurs in both seropositive and seronegative patients as the virus can cause reactivation and reinfection.[5] Hence, it may not be enough to avoid primary infection in those patients who have been identified as CMV negative; CMV-positive patients would also benefit from CMV­negative blood products as the virus within the transfused blood may cause severe recurrence of the disease in patients with extremely compromised immunity. Therefore, the use CMV-free blood products only in CMV-seronegative patients should be carefully reconsidered.

 ¤ Summary Top

The seroprevalence of cytomegalovirus (CMV) infection was determined among 584 volunteer mauritian blood donors using the complement fixation test (CFT) and a panel of CMV­seronegative blood donors was established. Blood samples were collected from 551 males and 33 females aged between 18 and 60 years. The prevalence of CMV­antibodies was found to be 93.5% with 93.1 % in males and 100% in females. The very high prevalence of CMV infection observed in our study indicated that it would be advisable to use leucocyte-depleted blood whenever CMV-seronegative blood was mandatory during blood transfusions.


Objective :
To determine the seroprevalence of CMV antibodies in the Mauritian volunteer blood donor population and to establish a panel of CMV-seronegative blood donors.

Study subjects and methods: Five hundred and eighty four apparently healthy blood donors were screened for evidence of CMV infection by the complement fixation test. There were 551 males and 33 females with age ranging from 18 to 60 years.

Results: Complement-fixing antibodies were found in 93.5% of the blood donors. The prevalence was 93.1% in males and 100% in females.

Conclusion: Our findings demonstrate that seroprevalence of CMV in the local blood donors is very high making CMV-seronegative blood very scarce. Therefore leucocyte-depleted blood should be used as an alternative to CMV­seronegative blood during transfusions.

 ¤ Acknowledgements Top

The authors would like to thank the Ministry of Health and the Blood Bank of Mauritius. We are very grateful to the people who participated in the survey. We also express our gratitude to the staff of the virology laboratory, especially V. Pursem, H. Mathur, S. Emrith, and V Appadoo for their co-operation. The Tertiary Education Commission (TEC) is thanked for financial support of part of this project.

 ¤ References Top

1.Chopra HL. Textbook of medical microbiology, pp. 632-633, New Delhi, Seema Publications, 1985.  Back to cited text no. 1    
2.Zukermann Aj, Banatvala JE Pattison JR. Principles and practice of clinical virology (3rd ed). pp. 68­108, West Sussex, John Wiley & sons Ltd, 1995.  Back to cited text no. 2    
3.Sharma R Bahl I, Goyal A, Sharma A, Sharma M. Thakur JS. Congenital cytomegalovirus infection in Shimla hills, Himachal Pradesh, India. J Commun Dis 1995;27:23-26.  Back to cited text no. 3    
4.Schimdt NJ, Emmons RW. Diagnostic procedures for viral, rikettsial and chamydial infections, pp. 321-379, Washington, American Public Health Association, 1985.  Back to cited text no. 4    
5.Larrsson S, Soderberg-Naucler C, Wang FZ, Moller E. Cytomegalovirus DNA can be detected in peripheral blood mononuclear cells from all seroposive and most seronegative healthy blood donors over time. Transfusion 1998;38:271-278.  Back to cited text no. 5    
6.Dejong MD, Galasso GJ, Gazzard B, Griffiths PD, Jabs D, et al. Summary of the II international symposium on cytomegalovirus. Antiviral Research 1998;39:141-­162.  Back to cited text no. 6    
7.Kreel I, Zaroff LI, Canter JW, Krasna I, Baronofsky ID. A syndrome folloing total body transfusion Surgery Gynaecology Obstetrics 1960;3:317.  Back to cited text no. 7    
8.Kaarianen I, Kiemola E, Paloheimo J. Rise of infectious antibodies in an infectious-mononucleosis-like syndrome after transfusion British med J 1966;1:1270-1272.  Back to cited text no. 8    
9.Tegtmeier GE. Post transfusion cytomegalovirus infections. Arch Pathol lab Med 1959;113:236-245.  Back to cited text no. 9    
10.Urwijitaroon Y, Teawpatanataworn S, Kijareontarm A. Prevalence of cytomegalovirus antibody in Thai­northeastern blood donors. Southeast Asain J Trop Med Public Health 1993;24:180-182.  Back to cited text no. 10    
11.Stroffolini T, Ngatchu T, Chiaramonte M, Gimmanco A, Maggio M, et al. Prevalence of cytomegalovirus seropositivity in an urban childhood population in Cameroon. New Microbiol 1993;16: 83-85.  Back to cited text no. 11    
12.Prabhakar P, Bailey A, Smickle MF, McCaw-Binns A, Ashley D. Seroprevalence of toxoplasma gondii, rubella virus, cytomegalovirus, herpes simplex virus (TORCH) and syphilis in Jamaican pregnant women. West Indian med J. 1991;40:166-169.  Back to cited text no. 12    
13.Krech U. Complement-fixing antibodies against cytomegalovirus in different parts of the world Bull WHO 1973;49:103-106.  Back to cited text no. 13    
14.Kubo T, Rai SK, Nakanishi M, Yamano T. Seroepidemiological study of herpes viruses in Nepal. Southeast Asian J Trop Med Public Health 1991;22:323-325.  Back to cited text no. 14  [PUBMED]  
15.Wentworth BB, Alexander ER, Seroepidemiology of infections due to members of the herpesvirus group. Am J Epidemiol 1971;14:496-507.  Back to cited text no. 15    


[Table - 1]

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