Evidence defense mechanism against viruses. Increasing virus

Evidence suggests that autophagy plays an
important role in the removal of patches. Overexpression of
beclin 1 in neurons using a Sindbis virus expression vector reduced Sindbis virus
replication (Liang et al., 1998). In addition, in cells isolated from beclin 1
or atg5 mutants, Sindbis virus and herpes simplex virus replicate to higher
titres than in wildtype cells (Levine and Yuan, 2005; Seay et al., 2005). Similarly,
plant virus TMV in Beclin 1-silenced plants accumulate more than wild-type plants
(Liu et al., 2005). These
results suggest that autophagy acts as a defense mechanism against viruses. Increasing virus accumulation in
autophagy deficiency cells indicates that the ATG protein may target the
cellular factors or pathways required to replicate and spread the virus (Liu et al., 2005). It seems that some bacteria have strategies to
counter-defence for eliminate autophagy and promote a successful infection (Ogawa
et al., 2005). For example, ATG5 interacts directly with the VirG protein
encoded by Shigella flexneri and targets bacteria for destruction. However, the
Shigella encoded effector protein IcsB interferes with this recognition. Mutant
Shigella lacking IcsB by autophagosomes are engulfed and targeted for
destruction (Ogawa et al., 2005). Recent evidence Showed that the mechanism of
autophagy initiated by HR-PCD during plant innate immunity is controlled (Liu
et al ., 2005). The tobacco N protein belongs to the TIR-NB-LRR
(toll/interleukin-1 receptor homology domain/nucleotide binding site/leucine
rich protein) class of R proteins and confers resistance to tobacco mosaic
virus (TMV) (Whitham et al ., 1994). The N protein specifically recognizes the
50 kDa helicase domain of the TMV replicase protein to induce HR-PCD and limit
the spread of the virus. To identify genes that control N-mediated
HR-PCD, Liu et al. (2005) a high-power RNAi display is produced. Interestingly,
silencing of Beclin 1 Causein uncontrolled HR-PCD against TMV infection (Fig. 4).
This phenotype is dependent on a successful innate immune response because Beclin1-silenced
plants infected with TMV unsuccessful to cause death in the absence of N. Interestingly,
silencing of other autophagy genes including PI3K/VPS34, ATG3 and ATG7 also resulted
in non-HR-PCD control of TMV infection (Liu et al., 2005).