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Abstract
Tula hantavirus carrying recombinant S RNA segment (recTULV) grew in a cell culture to the same titers as the original cell adapted variant but presented no real match to the parental virus. Our data showed that the lower competitiveness of recTULV could not be increased by pre-passaging in the cell culture. Nevertheless, the recombinant virus was able to survive in the presence of the parental virus during five consecutive passages. The observed survival time seems to be sufficient for transmission of newly formed recombinant hantaviruses in nature.
Highlights
Recombination in RNA viruses serves two main purposes: (i) it generates and spreads advantageous genetic combinations; and (ii) it counters the deleterious effect of mutations that, due to the low fidelity of viral RNA polymerases and lack of proofreading, occur with high frequency [1]
We have shown transfection-mediated rescue of Tula hantavirus (TULV) with recombinant S segment, in which nt 1–332 originate from the cell culture isolate Moravia/Ma5302V/ 94 [18], nt 369–1853 originate from the strain Tula/Ma23/87 [19], and nt 333–368, that are identical in both variants, can be of either origin
We designed Reverse transcription (RT)-polymerase chain reaction (PCR) primers able to discriminate between non-recombinant (V-type) and recombinant (REC-type) types of TULV S RNA
Summary
Recombination in RNA viruses serves two main purposes: (i) it generates and spreads advantageous genetic combinations; and (ii) it counters the deleterious effect of mutations that, due to the low fidelity of viral RNA polymerases and lack of proofreading, occur with high frequency [1]. HRec was first described for the positive-sense RNA viruses [2,3] and subsequent studies lead to the widely accepted copychoice model [4]. HRec was later shown to occur in rotaviruses adding double-stranded RNA viruses to the list of viruses capable of recombination [5]. Negativesense RNA viruses that occupy the largest domain in the virus kingdom until recently were known to undergo nonhomologous recombination only, forming either defective genomes, like polymerase "mosaics" of influenza A virus DI-particles [6] and "copy-backs" of parainfluenza virus [7] or hybrids between viral and cellular genes [8] or between different viral genes [9]. The first evidence for HRec in a negative-sense RNA virus has been obtained on hantaviruses [10,11]
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