High Expression of FcγII (CD32) Receptor on Monocytes in Dengue Infected Patients

Umi Solekhah Intansari, Harina Salim, Usi Sukorini, Adika Zhulhi Arjana, Muhammad Juffrie

Abstract


BACKGROUND: Pathogenesis of severe dengue infection has not been elucidated. Immune complex of pre-existing antibodies and heterotypic dengue virus bind to FcγII (cluster of differentiation (CD32)) receptor (FcγIIR) on monocyte facilitates entry and replication of dengue virus. Aim of this study was to evaluate the expression of FcγIIR on monocytes in patients infected with dengue and in healthy subjects.

METHODS: This study used a cross-sectional design that included patients infected with dengue who were hospitalized in Dr. Sardjito General Hospital, Panembahan Senopati Hospital, and Sleman Hospital, who met the inclusion criteria and selected consecutively. Examinations were completed using a lyse, no-wash method of flow cytometry. Computerized statistical analysis was conducted and was considered to be significant if p<0.05.

RESULTS: Sixty-five study subjects were divided into healthy subjects (24 subjects) and patients with dengue infection (41 subjects). There were no significant differences in hemoglobin (Hb) and hematocrit (Hct) values between the groups, but differences were found in the number of leukocytes, absolute number of monocytes and platelet count (p<0.001, 0.002 and <0.001, respectively). The mean expression of FcγIIR monocytes in patients with dengue infection (208.77±32.06 median fluorescent intensity (MFI)) and the healthy subjects (124.03±47.76 MFI) with p<0.0001.

CONCLUSION: The mean expression of FcγIIR monocytes in patients with dengue infection was higher than in healthy subjects.

KEYWORDS: dengue infection, FcγII (CD32) receptor monocyte, flow cytometry


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References


Malavige, GN, Fernando S, Fernando, DJ, Seneviratne SL. Dengue viral infections. Postgrad Med J. 2004; 80: 588-601, CrossRef.

Martina BEE, Koraka P, Osterhaus ADME. Dengue virus pathogenesis: an integrated view. Clin Microbiol Rev. 2009; 22: 564-81, CrossRef.

Kementerian Kesehatan RI. Demam berdarah dengue. Buletin Jendela Epidemiologi. 2010; 2: 1-15, article.

Blackley S, Kou Z, Chen H, Quinn M, Rose RC, Schlesinger JJ, et al. Primary human splenic macrophages, but not T or B cells, are the principal target cells for dengue virus infection in vitro. J Virol. 2007; 81: 13325-34, CrossRef.

Clyde K, Kyle JL, Harris E. Recent advances in deciphering viral and host determinants of dengue virus replication and pathogenesis. J Virol. 2006; 80: 11418-31, CrossRef.

World Health Organization. Comprehensive Guideline for Prevention and Control for Dengue and Dengue Haemorrhagic Fever. Revised and expanded edition. Geneva: WHO; 2011, article.

Wati S, Li P, Burrell CJ, Carr JM. Dengue virus (DV) replication in monocyte-derived macrophages is not affected by tumor necrosis factor alpha (TNF-alpha), and DV infection induces altered responsiveness to TNF-alpha stimulation. J Virol. 2007; 81: 10161-71, CrossRef.

Kou Z, Quinn M, Chen H, Rodrigo WW, Rose RC, Schlesinger JJ, et al. Monocytes, but not T or B cells, are the principal target cells for dengue virus (DV) infection among human peripheral blood mononuclear cells. J Med Virol. 2008; 80: 134-46, CrossRef.

Torsteinsdottir I, Arvidson NG, Hallgren R, Håkansson L. Monocyte activation in rheumatoid arthritis: increased integrin, Fcγ and complement receptor expression and the effect of glucocorticoids. Clin Exp Immunol. 1999; 115: 554-60, CrossRef.

Veri MC, Gorlatov S, Li H, Burke S, Johnson S, Stavenhagen J, et al. Monoclonal antibodies capable of discriminating the human inhibitory FcγRIIB (CD32B) from the activating FcγIIA (CD32A): biochemical, biological and functional characterization. Immunology. 2007; 121: 392-404, CrossRef.

García G, Sierra B, Pérez AB, Aguirre E, Rosado I, Gonzalez N, et al. Asymptomatic dengue infection in a Cuban population confirms the protective role of the RR variant of the FcgammaRIIa polymorphism. Trop Med Hyg. 2010; 82: 1153-6, CrossRef.

Intansari US, Sukorini U, Sari SI. FcγRII (CD32) Monocytes in primary and secondary dengue infection. Indones J Clin Pathol Med Lab. 2015; 22: 42-7, article.

Hottz E, Tolley ND, Zimmerman GA, Bozza FA. Platelets in dengue infection. Drug Discov Today Dis Mech. 2011; 8: e33-8, CrossRef.

Kalayanarooj S, Vaughn DW, Nimmannitya S. Early clinical and laboratory indicators of acute dengue illness. J Infect Dis. 1997; 176: 313-21, CrossRef.

Rubio GD, Torno LL. Association of leukocyte and thrombocyte counts as a predictor of bleeding outcomes among dengue patients. Phil J Microbiol Infect Dis. 2007; 36: 33-8.

Soegijanto S. Patogenesa dan Perubahan Patofisiologi Infeksi Virus Dengue. Surabaya: Airlangga University Press; 2008.

Seneviratnea SL, Malavige GN, de Silva HJ. Pathogenesis of liver involvement during dengue viral infections. Trans R Soc Trop Med Hyg. 2006; 100: 608-14, CrossRef.

Srikiatkhachorn A. Plasma leakage in dengue haemorrhagic fever. Thromb Haemost. 2009; 102: 1042-9, CrossRef.

Anderson R, Wang S, Osiowy C, Issekutz IC, et al. Activation of endothelial cells via antibody enhanced dengue virus infection of peripheral blood monocytes. J Virol. 1997; 71: 4226-32, article.

Suharti C. Dengue Hemorrhagic Fever in Indonesia: The Role of Cytokines in Plasma Leakage, Coagulation and Fibrinolysis [Dissertation]. Netherland: Nijmegen Universiteit; 2001.

Durbin AP, Vargas MJ, Wanionek K, Hammond SN, Gordon A, Rocha C, et al. Phenotyping of peripheral blood mononuclear cells during acute dengue illness demonstrates infection and increased activation of monocytes in severe cases compared to classic dengue fever. Virology. 2008; 376: 429-35, CrossRef.




DOI: https://doi.org/10.18585/inabj.v10i3.434

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