Poa Semilatent Virus from Native Grasses. J. T. Slykhuis, Ottawa Research Station, Research Branch, Canada Department of Agriculture, Ottawa, Ontario; Phytopathology 62:508-513. Accepted for publication 15 July 1971. DOI: 10.1094/Phyto-62-508.
Poa semilatent virus (PSLV), discovered in Poa palustris and Agropyron trachycaulum from Alberta, Canada, caused mosaic, chlorosis, and blight on wheat (Triticum aestivum) and oats (Avena sativa), but only a mild transitory mottling on P. palustris. Other hosts include Agropyron cristatum, Alopecurus aequalis, Avena (16 spp), Elymus canadensis, Hordeum marinum, H. vulgare (11 cultivars), Lolium multifluorum, Phleum pratense, Poa compressa, Secale cereale, Triticum durum, and Zea mays.
The original isolate killed most wheat plants 2-3 weeks after inoculation. Nonlethal isolates were segregated from the lethal isolate, but when recombined in transmission tests, they suppressed the lethal effects of the latter on wheat.
Wheat and oat plants became infected when grown in pots of soil with naturally infected P. palustris. No infection occurred in tests for soil and seed transmission.
Highest infectivity and serological titers were obtained with juice from leaves that were 50% chlorotic. The virus was infectious in wheat juice at pH 4 to 10. Heat inactivation occurred between 65 and 67.5 C. Infectivity was lost in 2-4 months in juice and undried leaves stored in vials at 20, 5, or –15 C, but was undiminished after 1 year in leaves stored over CaCl2 at –15 C.
Particles in dip preparations from plants infected with PSLV were stiff rods 25 nm in diam and 125-225 nm long, with a mean normal length of 162 nm, compared to 133 nm for barley stripe mosaic virus (BSMV). An antiserum prepared for PSLV had a precipitation dilution end point of 1/8,192 against PSLV, and 1/64 against BSMV. Absorption of either antiserum with the heterologous virus did not reduce its titer against the homologous virus.