Host - Virus Interactions
Authors: Suneha Goswami and Amit Kumar Goswami
Indian Agricultural Research Institute-110012
The co-existence of viruses with their hosts can be viewed as a molecular arms race between the virus and host elimination mechanisms. Virus infections are the cause of numerous plant disease syndromes that are generally characterized by the induction of disease symptoms such as developmental abnormalities, chlorosis, and necrosis. Recent studies indicate that symptoms are derived from specific interactions between virus and host components. Although resistance to and recovery from viral infections will depend on the interactions that occur between virus and host. The defences mounted by the host may act directly on the virus or indirectly on virus replication by altering or killing the infected cell. The non-specific host defences function early in the encounter with virus to prevent or limit infection while the specific host defences function after infection in recovery immunity to subsequent challenges. Although the host defence mechanisms involved in a particular viral infection will vary depending on the virus, dose and portal of entry. Chromatin structure and histone modifications play key roles in gene regulation. Some virus genomes are organized into chromatin-like structure, which undergoes different histone modifications facilitating complex functions in virus life cycles including replication (Shanshanei al., 2014).
Higher plants are often subjected to multiple virus infections resulting in intensification of symptoms expression and virus accumulation which establish a host -virus interaction, a phenomenon known as synergism (Hull, 2002). In synergistic host-viral interaction, co-infection with two or more independent unrelated viruses results in a much more serious disease than either virus induces in a single infection (Matthews, 1991). RNA silencing suppressors from different plant viruses are structurally diverse. In addition to inhibiting the antiviral silencing response to condition susceptibility, many suppressors are pathogenicity factors that cause disease or developmental abnormalities. Systemic infection by plant viruses frequently results in disease symptoms that resemble developmental defects, including loss of leaf polarity, loss of proper control of cell division, and loss of reproductive functions (Hull 2002).
Unrelated suppressors from multiple viruses were shown to inhibit microRNA (miRNA) activities and trigger an overlapping series of severe developmental defects in transgenic Arabidopsis thaliana (Elisabethet al., 2004). This suggests that interference with miRNA-directed processes may be a general feature contributing to pathogenicity of many viruses. Plant miRNAs are involved in plant development, signal transduction, protein degradation and response to environmental stress and pathogen invasion. Viruses are known to exploit the host nucleic acid as a part of their infection strategy. miRNA mediated gene silencing serves as a general defence mechanism against plant viruses, it would not be a surprise that viruses also employ miRNA to circumvent the defence system.
The viral silencing suppressor can help viruses at an early stage of infection. P1/HC-Pro has been found to act as a suppressor of virus-induced gene silencing through targeting RISC (Anandlakshmiet al., 1998). The potyviralHc-Pro interferes with miRNA and siRNA pathways (Wu et al., 2010). In general, viruses accomplish counter-defence by targeting RNAs (Quetal., 2003) or protein (Anandalakshmiet al., 2000). Therefore, expression of host genes is modiﬁed or silenced (Dong et al., 2003). Recent ﬁndings suggest that silencing suppressors can contribute to viral symptoms in two ways: helping virus accumulation indirectly and modifying endogenous short-RNA-regulated pathways directly (Silhavy and Burgyan 2004).
Due to viral infection the level of microRNAs expression altered which affects the developmental biology of the host in the form of symptoms. In potyvirus associated synergism, the synergy include a potyvirus and a non potyvirus as a pair which may be of a broad range of unrelated viruses, including potexvirus, Potato virusX (PVX) in tobacco (Vance et al., 1995), machlovirus, Maize chlorotic mottle virus in maize (Goldberg et al., 1987), comoviruses, Bean pod mottle virus and Cowpea mosaic virus in soybean (Anjoset al., 1992), polerovirus, Potato leafroll virus in Nicotianaclevelandis, cucumovirus, Cucumber mosaic virus (CMV) in cucurbits and radish (Zenget al., 2007), crinivirus, Sweet potato chlorotic stunt virus in sweet potato (Untiveroset al., 2007). In most of these interactions, the increase in symptoms is correlated with an increase in accumulation of non potyvirus of the synergistic pair, but the corresponding increase or decrease in the level of potyvirus, was not observed (Prusset al., 1997).The extent to which the synergistic viral interactions occur in higher plants and role they play in mediating plant disease is not clear at this point. Moreover the basic background information about genes responsible for plant viral synergism is deficient.
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