The Molecular Mechanism of Antigenic Variation

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Abstract

Antigenic variation is an immune response generated strategy and has explored with respect to the viral, bacteria, protistans pathogens, and other diverse group of eukaryotic microorganisms. However, in African trypanosome, this antigenic variation is based on the changes in the composition of variant surface glycoprotein (VSG) coat. The VSG genes have the potential to change the characteristics of a single gene of VSG at a moment in time. This switching and expressing of genes of VSG has been processed by recombinant scientific reactions. Through these recombinant techniques silent genes of VSG have become expressive genes. Studies show that this molecular mechanism in antigen variation is utilizing the genetic tools of RNA interference, which can be further explored to analyze the regulation of VSG genes. In the mean while, transcription based switching of genes can also occur. This switching reaction of VSG genes can help the pathogen to survive in the form of several immune attacks of chronic infections which even lead to the phenomenon of host-host transmission.

Tables of Contents

Abstract2

Introduction4

Discussion5

Variant Surface Glycoprotein (VSG)5

Telomeric Expression Site for VSG6

Expression-linked Copies (ELCs) of VSG7

Mosaic Gene Expression in Antigenic Variation7

Differential RNA Elongation Controls8

Chromatin-Remodeling, Histone Proteins and Histone Methyltransferase8

Control of VSG Expression Site9

Theories Related to Antigenic Variation10

Conclusion11

References12

Appendices16

The Molecular Mechanism of Antigenic Variation

Introduction

Antigen variation is a genetic process through which pathogens can escape from immune reactions which is taken place in the hosts by changing their genetic expressions of surface antigens. Many pathogens must have the capability to complete one or more stages of their life cycle, while many of these pathogens have the ability to establish long term relationship with the host body in the form of chronic infections. Antigens which are foreign to the body are rapidly and effectively targeted by the immune system of the host body. In order to survive in such critical circumstances, these pathogens have developed the resistance against such immune mechanisms. This immune resistance is frequently changing the conformation of determinants of antigens. Therefore, for thrashing this genetic mechanism, the pathogen must possess the ability to transform its antigenic profile by introducing different variants at specific intervals. Furthermore, different mechanisms have been evolved that encourage this variation within genes which are responsible for altering the coding of surface proteins. These mechanisms are divided into two type random variation and programmed variation. Random variation utilizes the imperfections of Deoxyribonucleic acid (DNA) repairing due to mutations and variations in replication processes. While programmed variation involves the appearance of some unique mechanisms which can bring diversity in genes. In this process only one promoter is active at a time while the remaining genes stay behind the active promoter in downstream.

Antigenic variation is the primary reason for the perseverance and lethal activities of African trypanosome infections. Many viruses, bacteria, and other parasites have developed the mechanism by which these pathogens can invade immune systems. On the other hand, these pathogens are destroyed by the antibodies and T-cells. Similarly, most of the flows of trypanosomes are ...