the pathogenesis and clinical spectra of wupyv and kipyv , particularly in immunocompromised persons , have not been defined . to investigate whether wupyv or kipyv is present in persons with chronic viral infection and perhaps compromised immunity , we conducted a cross - sectional study in which we screened the following for wupyv and kipyv dna : plasma samples from hiv - infected persons , serum samples from hepatitis c virus ( hcv)infected persons , and a control group of hiv - negative persons . three groups of samples submitted to the clinical virology laboratory at yale  new haven hospital in 2007 were screened : hiv pcr - positive plasma , hcv pcr - positive serum , and hiv antibody - negative serum . patient identifiers were removed and these specimens were tested as part of our ongoing investigation for newly identified viruses . collection of specimens and clinical data was approved by the yale university human investigation committee and was compliant with health insurance portability and accountability act regulations . nucleic acids were extracted from each specimen by using qiaamp nucleic acid purification kits ( qiagen , valencia , ca , usa ) . briefly , we performed an initial pcr screening specific for the virus capsid protein 2 ( vp2 ) gene by using primers described by gaynor et al . ( 2 ) and a nested pcr ( table 1 , primers 1 and 2 ) . to confirm results , dna from all pcr - positive samples was reextracted and screened with primers specific for the region of the genome containing the noncoding control region ( nccr ) , which includes the virus origin of replication ( genome coordinates 5213 to nt 36 of the circular viral genome ) . this screening included an initial pcr ( table 1 , primers 3 and 4 ) and a nested pcr ( table 1 , primers 5 and 6 ) . screening for kipyv dna by pcr included a nested pcr specific for the vp1 gene according to the protocol described by allander et al . positive and negative controls were included in each set of pcrs . * primers used by wattier et al . the amplicon generated with these primer spans across nt 1 of the 5,229-bp circular virus genome . all pcr products were sequenced by using 377 dna automated sequencers ( applied biosystems , foster city , ca , usa ) at the w.m . , phylogenetic analysis was performed on a 194-bp fragment within the amplified region of nccr ( nt 5197 to nt 159 of the circular viral genome ) by using lasergene megalign software ( dnastar inc . , the only clinical data available for these deidentified serum specimens were hiv / hcv status and virus loads . hiv and hcv virus loads were determined in the clinical virology laboratory by quantitative reverse transcription  pcr using commercially available diagnostic tests . the fisher exact test was used to determine whether the difference in the percentage of wupyv - positive specimens in hiv - positive and hiv - negative patients was statistically significant . ten ( 8.3% ) of 121 hiv - positive specimens and 0 ( 0% ) of 120 hiv - negative samples were positive for wupyv ( p<0.01 ) ( table 2 ) . one of the 10 wupyv - positive , hiv - positive specimens was also positive for hcv . current hiv status for 2 of the wupyv - positive , hcv - positive persons was not available . none of the hiv - positive or hcv - positive specimens screened were positive for kipyv ( table 2 ) . mean hiv loads for wupyv - positive and wupyv - negative , hiv - positive persons were 32,200 copies / ml ( range 2,93088,300 copies / ml , median 25,100 copies / ml ) and 131,500 copies / ml ( range 509750,000 copies / ml , median 59,600 copies / ml ) , respectively . mean hcv loads for wuv - positive and wuv - negative persons were 1,302,200 copies / ml ( range 88,6003,906,600 copies / ml , median 1,909,000 copies / ml ) and 3,091,000 copies / ml ( range 2,03032,800,000 copies / ml , median 1,150,000 copies / ml ) , respectively . amplified sequences from wupyv - positive serum specimens were compared with available sequences from genbank ( all of which were obtained from respiratory specimens ) . several nucleotide polymorphisms were observed in the amplified portion of the nccr of the new haven wupyv serum isolates ( figure ) . none of the nucleotide changes in the new haven strains were mapped to the 4 putative large t - antigen binding sites within the origin of replication ( 2 ) . nucleotide polymorphisms in the noncoding region of wu polyomavirus ( wupyv ) , connecticut , usa , 2007 . sequences spanning nt 5197 to 159 of the circular viral genome of new haven human serum isolates and all available sequences from genbank ( all from respiratory specimens ) were subjected to phylogenetic analysis . a map of the noncoding region within the viral genome is indicated at the top of the figure ( not to scale ) . the arbitrary last ( 5229 ) and first ( 1 ) nucleotide of the circular viral genome are indicated . the putative large t antigen ( tag ) binding sites for each strand of the double - strand genome are indicated by black boxes , and the a / t - rich region is indicated by a gray box . strains ( location and genbank accession nos . ) are listed in order according to phylogenic analysis . the strain indicated by the black arrow is a wupyv new haven respiratory isolate ( 6 ) , and the strain indicated by the white arrow is the original wupyv isolate ( 2 ) . we detected wupyv in plasma specimens from hiv - infected persons and in serum specimens from hcv - infected persons in connecticut in 2007 . detection of wupyv indicates that this newly identified polyomavirus is present in peripheral blood of hiv - positive or hcv - positive persons . however , if the seroepidemiology of wupyv is similar to that of bkv and jcv , we predict that > 85% of the persons screened will have detectable antibodies to wupyv ( 11 ) . however , blood from viremic persons infected with jcv has a low positive predictive value for development of progressive multifocal encephalopathy in aids patients ( 9 ) . a recent study suggested that screening for bkv replication is useful in identifying patients at risk for bkv - associated nephropathy , which may enable early interventions such as renal biopsy and reduction of immunosuppression ( 12 ) . however , because of the lack of clinical data available for wupyv - positive persons in our study , it was not possible to make any clinical correlations . the absence of kipyv in hiv - positive or hcv - positive peripheral blood specimens suggests that host susceptibility for kipyv may differ from that of wupyv , as for jcv and bkv . however , this hypothesis was not supported by a recent study that reported kipyv and wupyv in autopsy lymphoid tissues of aids patients ( 13 ) . whether wupyv or kipyv cause disease in hiv - positive persons or other populations remains to be determined . our data demonstrate that wupyv was detected in peripheral blood of hiv- and hcv - infected persons . however , the scope of this study was limited because clinical data were not available for study participants . whether wupyv or kipyv have oncogenicity or other pathogenicity in immunocompromised hosts remain to be determined . the role of polyomaviruses in human cancers has been extensively investigated but conclusive evidence is lacking ( 14 ) . the genome of merkel cell polyomavirus , a new polyomavirus , was found to be integrated within the cellular genome of merkel cell carcinoma tissue samples , which suggests a role for this virus in a specific tumor ( 15 ) . therefore , studies to assess the oncogenic potential of wupyv and kipyv are also needed .
wu polyomavirus ( wupyv ) was detected in 10 ( 8.3% ) of 121 hiv - positive plasma specimens , 0 ( 0% ) of 120 hiv - negative serum specimens , and 2 ( 2.5% ) of 79 hepatitis c virus ( hcv)positive serum specimens . 
 ki polyomavirus was not detected in hiv - positive plasma or hcv - positive serum specimens . 
 hiv - infected persons may be susceptible to systemic wupyv infection .