Plant virus infection often disrupts host traits that are critical in responding to environmental stresses such as pigment accumulation. However, in natural ecosystems, plants have often been infected with plant viruses for long periods of time without showing critical damage. We hypothesized that plants can compensate for the negative effect of virus infection on their growth and survival by adjusting other functional traits. An evergreen perennial, Arabidopsis halleri, infected with Turnip mosaic virus (TuMV) can survive in the natural population for three or more years without showing severe symptoms. TuMV infection cause a marked inhibition of cold-induced anthocyanin accumulation in host individuals. Although anthocyanin accumulation is known to be involved in photoprotection of plants, infected A. halleri, which lacks anthocyanin accumulation, does not necessarily suffer from severe photoinhibition under natural condition. In order to investigate if and how the plant compensates for low anthocyanin accumulation, we conducted a sequential quantification of photoprotection-related traits under controlled conditions in the laboratory. Arabidopsis halleri plants grown at 25/25Cº (12/12h L/D) accumulated anthocyanin in their leaves within 4 weeks of chilling at 5/5Cº (12/12h L/D). Foliar anthocyanin concentration was significantly lower in TuMV-infected plants than in uninfected plants. We found that photoprotection capacity (F_v/F_m after highlight treatment) was significantly lower in TuMV-infected plants than in uninfected plants after 2 weeks of chilling treatment, whereas it was similar in both infected and uninfected plants after 4 weeks of treatment, suggesting that induction of photoprotection during cold acclimation occurs in TuMV-infected plants at the same level as uninfected plants, but the rate of induction is slower. We also found that infected plants with lower anthocyanin accumulation have significantly lower photodamage resistance (1/K_pi) than uninfected plants but have high repair rate of damaged PSⅡ (K_rec) after 4 weeks. These result suggests that the induction of PSⅡ repair compensates for the total photoprotection ability in infected plants. We further conducted a field experiment at the end of January and observed similar phenomenon that TuMV infection significantly reduce photodamage resistance (1/K_pi) but does not change total photoprotection (F_v/F_m). Our results suggest that A. halleri can alleviate a negative effect of TuMV-induced inhibition of anthocyanin accumulation by adjusting repair rate of PSⅡ and maintain its photosynthetic capacity during the winter season. However, infected plants may be damaged when the air temperature drops suddenly because the induction rate of photoprotection during cold acclimation is slowed by TuMV infection.