Genetic differences between human immunodeficiency virus type 1 subpopulations in faeces and serum.

Hoek, Lia van der; Sol, C. J. A.; Maas, Jolanda; Lukashov, Vladimir V.; Kuiken, Carla; Goudsmit, Jaap

doi:10.1099/0022-1317-79-2-259

Cited by 12 publications

(8 citation statements)

References 37 publications

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“…The performance of VIDISCA-454 in feces was investigated using broth suspensions from a sample-bank collected from HIV-1 infected individuals in 1994 and 1995 [8]. A norovirus infection was diagnosed in five people via real time RT-PCR [9], the viral load in feces suspension ranged between 5 × 10 3 and 3 × 10 7 genome copies/mL.…”

Section: Resultsmentioning

confidence: 99%

Performance of VIDISCA-454 in Feces-Suspensions and Serum

Vries

Munnink

Deijs

et al. 2012

Viruses

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Virus discovery combining sequence unbiased amplification with next generation sequencing is now state-of-the-art. We have previously determined that the performance of the unbiased amplification technique which is operational at our institute, VIDISCA-454, is efficient when respiratory samples are used as input. The performance of the assay is, however, not known for other clinical materials like blood or stool samples. Here, we investigated the sensitivity of VIDISCA-454 with feces-suspensions and serum samples that are positive and that have been quantified for norovirus and human immunodeficiency virus type 1, respectively. The performance of VIDISCA-454 in serum samples was equal to its performance in respiratory material, with an estimated lower threshold of 1,000 viral genome copies. The estimated threshold in feces-suspension is around 200,000 viral genome copies. The decreased sensitivity in feces suspension is mainly due to sequences that share no recognizable identity with known sequences. Most likely these sequences originate from bacteria and phages which are not completely sequenced.

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Section: Resultsmentioning

confidence: 99%

Performance of VIDISCA-454 in Feces-Suspensions and Serum

Vries

Munnink

Deijs

et al. 2012

Viruses

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“…For example, different frequencies of antiviral resistant variants in gut mucosal biopsy samples with circulating virus in plasma were obtained from a minority of individuals (61). Similarly, V3 sequence differences were frequently found between variants of HIV recovered from feces and those found in peripheral blood (79,80).…”

Section: Fig 6 (A)mentioning

confidence: 99%

Identification of Shared Populations of Human Immunodeficiency Virus Type 1 Infecting Microglia and Tissue Macrophages outside the Central Nervous System

Wang

Donaldson

Brettle³

et al. 2001

J Virol

182

180

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Infection of microglia and other cells of the macrophage/monocyte lineage in the central nervous system (CNS) by human immunodeficiency virus type I (HIV-1) underlies the development of giant cell encephalitis (GCE). It is currently unknown whether GCE depends on the emergence of virus populations specifically adapted to replicate in cells of the monocyte/macrophage lineage and whether this also leads to the specific targeting of macrophages in other nonlymphoid tissues. Autopsy samples from lymph node, brain (frontal region), lung, and full-thickness colon sections were obtained from nine study subjects with GCE and from nine without. The two groups showed no significant differences in CD4 counts, disease progression, or treatment history before death. Genetic relatedness between variants recovered from lymph node and nonlymphoid tissues was assessed by sequence comparison of V3 and p17 gag regions using a newly developed method that scores the sample composition at successive nodes in a neighbor-joining tree. The association index enabled objective, numerical comparisons on the degree of tissue compartmentalization to be made. High proviral loads and p24 antigen expression in the brain were confined to the nine individuals with GCE. GCE was also associated with significantly higher proviral loads in colon samples (median of the GCE ؉ group: 1,010 copies/10 6 cells; median of GCE ؊ group, 10/10 6 cells; P ‫؍‬ 0.006). In contrast, there were no significant differences in proviral load between the GCE ؉ and GCE ؊ groups in lymph node or lung samples, where HIV infection was manifested predominantly by infiltrates of lymphoid cells. V3 sequences from brain samples of individuals with GCE showed the greatest compartmentalization from those of lymph node, although samples from other tissues, particularly the colon, frequently contained variants phylogenetically related to those found in brain. The existence of shared, distinct populations of HIV specifically distributed in cells of the monocyte/ macrophage lineage was further indicated by immunocytochemical detection of CD68 ؉ , multinucleated giant cells expressing p24 antigen in samples of lung and colon in two individuals with GCE. This study provides the basis for future investigation of possible phenotypic similarities that underline the shared distributions of HIV variants infecting microglia and tissue macrophages outside the CNS.

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“…A number of other studies examining lymphoid and nonlymphoid tissue compartments have also suggested compartmentalization of viral evolution (9,15,20,21,22,30,51). Though there have been few studies of HIV-1 evolution in the intestinal mucosa, genotypic differences in the env, pro, and reverse transcriptase genes of HIV-1 quasispecies in the intestinal mucosa and blood have been described (35,43,44). HIV-1 isolates from the gastrointestinal mucosa have also been shown to differ from paired blood isolates in terms of their ability to induce cytopathology in infected cells and showed a greater sensitivity to serum neutralization in one study (4).…”

Section: Ccr5mentioning

confidence: 99%

A Preponderance of CCR5⁺CXCR4⁺Mononuclear Cells Enhances Gastrointestinal Mucosal Susceptibility to Human Immunodeficiency Virus Type 1 Infection

Poles¹,

Elliott²,

Taing³

et al. 2001

J Virol

153

106

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The gastrointestinal mucosa harbors the majority of the body's CD4؉ cells and appears to be uniquely susceptible to human immunodeficiency virus type 1 (HIV-1) infection. We undertook this study to examine the role of differences in chemokine receptor expression on infection of mucosal mononuclear cells ( , while these cells make up less than 20% of the peripheral blood cells. It is this cell population that is most susceptible to infection with both R5-and X4-tropic HIV-1 in both compartments. Regardless of whether viral isolates were derived from the blood or mucosa of HIV-1-infected patients, HIV-1 p24 production was greater in MMCs than in PBMCs. Further, the chemokine receptor tropism of these patient-derived viral isolates did not differ between compartments. We conclude that, based on these findings, the gastrointestinal mucosa represents a favored target for HIV-1, in part due to its large population of CXCR4 ؉ CCR5 ؉ target cells and not to differences in the virus that it contains.

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Genetic differences between human immunodeficiency virus type 1 subpopulations in faeces and serum.

Cited by 12 publications

References 37 publications

Performance of VIDISCA-454 in Feces-Suspensions and Serum

Performance of VIDISCA-454 in Feces-Suspensions and Serum

Identification of Shared Populations of Human Immunodeficiency Virus Type 1 Infecting Microglia and Tissue Macrophages outside the Central Nervous System

A Preponderance of CCR5⁺CXCR4⁺Mononuclear Cells Enhances Gastrointestinal Mucosal Susceptibility to Human Immunodeficiency Virus Type 1 Infection

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Genetic differences between human immunodeficiency virus type 1 subpopulations in faeces and serum.

Cited by 12 publications

References 37 publications

Performance of VIDISCA-454 in Feces-Suspensions and Serum

Performance of VIDISCA-454 in Feces-Suspensions and Serum

Identification of Shared Populations of Human Immunodeficiency Virus Type 1 Infecting Microglia and Tissue Macrophages outside the Central Nervous System

A Preponderance of CCR5+CXCR4+Mononuclear Cells Enhances Gastrointestinal Mucosal Susceptibility to Human Immunodeficiency Virus Type 1 Infection

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A Preponderance of CCR5⁺CXCR4⁺Mononuclear Cells Enhances Gastrointestinal Mucosal Susceptibility to Human Immunodeficiency Virus Type 1 Infection