Viral Determinants of Resistance Versus Susceptibility

The 50 distal amino acids of the 2AHP homing protein of Grapevine fanleaf virus elicit a hypersensitive reaction on Nicotiana occidentalis

“…Alternatively, as protein 2A HP is involved in RNA2 replication (Gaire et al, 1999), and thus indirectly in encapsidation and movement, the host resistance gene could act directly by inhibiting virus replication and movement. However, many Avr factors act independently of virus accumulation (Hasi ow-Jaroszewska et al, 2011; Mansilla et al, 2009;Schoelz, 2006). Future experiments will aim to uncouple these two functions of GFLV protein 2A HP .…”

Plant Immune Responses Against Viruses: How Does a Virus Cause Disease?

“…These questions necessarily transition into an area of semantics that we suggest would likely benefit from some convergence, particularly when describing antiviral immune responses that are analogous to nonviral immune responses. For example, the R gene-mediated virus resistance involves specific recognition of virus-encoded Avr proteins that culminate in HR and SAR responses, as shown for TMV N gene resistance and others (Whitham et al, 1994;Liu et al, 2002a;Schoelz, 2006). However, it is unclear whether they can be classified as ETI responses because of the existing definition (or lack thereof) of what constitutes an effector protein for diverse pathogen types (i.e., viruses versus bacteria).…”

“…Furthermore, in the case of tobacco N-mediated resistance, the TMV-encoded p50 protein is recognized by the N protein and its cofactor NRIP1 to elicit the Nmediated host immune response (Caplan et al, 2008). These and several other instances reviewed in detail elsewhere (Schoelz, 2006) beg the following question: Should these virulence-promoting factors be referred to as effectors and the immune responses they trigger be classified as ETI responses? Based on the analogous functions of nonviral effector proteins, we propose a working definition for viral effectors: Viral effectors are virus-encoded proteins that when present in host cells interfere with host defense signaling components to promote virulence.…”

“…Earlier reviews discussing microbial effectors and their functional definitions noted that several bacterial and fungal avirulence factors are indeed "double agents" that can promote pathogenesis while eliciting ETI responses, suggesting that some avirulence proteins are also effectors (Alfano and Collmer, 2004;Schoelz, 2006). For example, the AvrPtoB protein of PstDC3000 can simultaneously suppress HR, as well as elicit ETI responses in the presence of the appropriate R gene, Pto (Abramovitch et al, 2003).…”

“…For example, the AvrPtoB protein of PstDC3000 can simultaneously suppress HR, as well as elicit ETI responses in the presence of the appropriate R gene, Pto (Abramovitch et al, 2003). As discussed above, several virusencoded Avr factors, such as CaMV P6 protein, can interfere with plant defense pathways while eliciting R-mediated resistance responses (Schoelz, 2006). According to our proposed definition for viral effectors, virus Avr factors that interfere with host defenses should thus be referred as effectors.…”