Results for harboured translation from English to Maltese

sixteen of 30 subjects (53%) harboured q148 virus at baseline.
sittax minn 30 individwu (53%) kellhom virus q148 fil-linja bażi.

victims are often recruited, transported or harboured by force, coercion or fraud.
il-vittmi spiss jiġu reklutati, trasportati jew alloġġjati bil-forza, il-kostrizzjoni jew il-frodi.

23-50-fold) harboured 2 to 4 amino acid substitutions in the protease gene.
23- 50 darba) kellhom fihom bejn 2 u 4 sostituzzjonijiet tal- aċidu amminiku fil- ġene protease.

tick species harboured by pets are widespread in europe, including in the uk, ireland and probably malta.
l-ispeċjijiet tal-qurdien li jgħixu fuq l-annimali domestiċi huma mifruxa sew fl-ewropa, inklużi r-renju unit, l-irlanda u probabilment malta.

according to the efsa, tick species harboured by pets are widespread in europe, including in the uk, ireland and probably malta.
skont l-efsa, l-ispeċi tal-qurdien li jgħixu fuq l-annimali domestiċi huma mifruxa sew fl-ewropa, inklużi fir-renju unit, fl-irlanda u probabilment f'malta.

conversions at position 80, 180 and polymorphic positions 91, 229 were always detected in sequences that harboured the m204i mutation that confers genotypic resistance.
seħħew konverżjonijiet f’pożizzjoni 80, 180 u f’pożizzjonijiet polimorfiċi 91, 229 li dehru dejjem f’sekwenza li pproteġiet il-mutazzjoni m204i li twassal għal reżistenza ġenotipika.

clinical isolates that exhibited a ≥ 10-fold decrease in tipranavir susceptibility harboured eight or more tipranavir-associated mutations.
il- kampjuni iżolati kliniċi li wrew tnaqqis ta '≥10 darbiet fis- suxxetabilità ta' tipranavir kellhom tmien mutazzjonijiet jew aktar assoċjati ma 'tipranavir.

tick species harboured by pets (i.e. dogs, cats, ferrets) and their distribution through europe have been itemised.
l-ispeċijiet tal-qurdien li jospitaw l-annimali domestiċi (jiġifieri klieb, qtates, inmsa) u t-tixrid tagħhom ma' l-ewropa ġew ikklassifikati.

patients who failed treatment with stribild and who had hiv-1 with emergent stribild resistance substitutions harboured virus that remained susceptible to all pis, nnrtis, and most other nrtis.
pazjenti b’trattament li ma rnexxietx bi stribild u li kellhom hiv-1 b’sostituzzjonijiet ta’ reżistenza li żviluppat għal stribild bil-virus li baqgħu suxxettibbli għal pis u nnrtis kollha, u l-biċċa l-kbira tal-nrtis l- oħrajn.

this subject harboured 99%) at 4 weeks post-treatment which resulted in a 13.5-fold change in sofosbuvir ec50 and reduced viral replication capacity.
dan l-individwu kellu 99%) 4 ġimgħat wara l-kura, li rriżultat f’bidla ta’ 13.5 drabi fl-ec50 ta’ sofosbuvir u naqqset il-kapaċità tar-replikazzjoni virali.

patients must not have experienced virological failure on any prior antiretroviral therapy and must be known not to have harboured virus strains with mutations conferring significant resistance to any of the three components contained in atripla prior to initiation of their first antiretroviral treatment regimen (see sections 4.4 and 5.1).
il- pazjenti ma jridux ikunu esperjenzaw falliment viroloġiku fuq xi terapija antiretrovirali preċedenti u jrid ikun magħruf li ma kellhomx forom tal-virus b’mutazzjonijiet li jagħtu reżistenza sinifikanti għal xi wieħed mit-tliet komponenti kontenuti f’atripla qabel ma jinbeda l-ewwel reġim ta’ trattament antiretrovirali tagħhom (ara sezzjoni 4.4 u 5.1).