Anukul Paul, Sriradha Ganguli and Ranadhir Chakraborty
OMICS Laboratory, Department of Biotechnology, University of North Bengal, Siliguri, West Bengal, India

Part of the book: Advances in Health and Disease. Volume 62

Abstract

Plasmids are DNA molecules that may replicate independently of chromosomal DNA and are found in a variety of prokaryotes and eukaryotes. Even though they aren’t a part of the bacterial genome, their presence is critical for bacterial survival and stability in adverse settings. The capacity of broad host range (BHR) plasmids to disseminate favourable genetic features among species as well as among taxonomically distant species is of great interest. The presence of genes that code for antibiotics and antibiotic hydrolyzing enzymes, toxic heavy metal resistance, radiation resistance, xenobiotic-compound degradation, virulence determinants, and bacteriocin production can all be ascribed to the calibre of plasmids. Plasmids can also carry the genetic information for a type IV secretion system, such as the tumour inducing (Ti) plasmid in virulent Agrobacterium tumefaciens, which is involved in gene transfer. Plasmids acquire mobile genetic elements (insertion sequences, transposons) that mobilise antimicrobial resistance genes and promote horizontal resistance determinant transfer among bacteria of various species and genera, depending on their host range, conjugative properties, and conjugation efficiency. In bacteria like Escherichia coli, Yersinia spp., and Shigella spp., plasmids encode virulence factors that are responsible for pathogenicity. The existence of virulence plasmids in pathogenic bacteria is ubiquitous, albeit the genetic composition and involvement at different stages of the disease vary by species. Virulence plasmids have a low copy number (10 per cell) but are big (>40 kb) and work similarly to episomal PAIs (Pathogenicity Islands) by undergoing internal remodelling and horizontal gene transfer. Certain virulence plasmids can also exchange virulence components with the genome or integrate with it, resulting in a genomic PAI. Viruses that cause African swine fever, such as the iridovirus, have structures that are similar to plasmids. Borrelia species cause Lyme disease and relapsing fever via their linear plasmids, which appear to encode both hemolysins, which harm blood cells, and surface proteins, which protect the bacteria from the host immune system. Restriction/anti-restriction mechanisms and partitioning systems are frequently encoded by promiscuous broad-range plasmids, ensuring sustained inheritance during bacterial cell division. These strategies encourage the persistence of plasmids while providing no advantage to the bacterial host. Purified plasmid DNA (pDNA) vaccines, on the other hand, have opened up new ways to treat emerging infectious pathogens like HIV (human immunodeficiency virus), SARS coronavirus (severe acute respiratory syndrome virus), and highly pathogenic avian influenza (H5N1) viruses that have evolved strategies to rapidly change their genetic compositions and for which other conventional vaccines have failed. A gene encoding an antigen of the target pathogen is included in a plasmid used in DNA vaccination (immunogen gene). A promoter “turns on” protein antigen expression in the host cell, and a terminator “turns it off” (a polyadenylation signal sequence). In our ever-changing microbial environment, plasmid DNA vaccines have the potential to improve human health by preventing diseases through immunization. Apart from all of these aspects, the current review will shed light on how plasmids contribute to pathogen virulence, the fitness cost they impose on their hosts, and how their coevolution with the host resolves the plasmid paradox, as well as how temperature affects the genetic plasticity of virulence plasmids.

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