Cells in Dengue Virus Infection In Vivo

Noisakran, Sansanee; Onlamoon, Nattawat; Songprakhon, Pucharee; Hsiao, Hui-Mien; Chokephaibulkit, Kulkanya; Perng, Guey Chuen

doi:10.1155/2010/164878

Cited by 65 publications

(46 citation statements)

References 136 publications

(152 reference statements)

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“…Figure 4 shows that the genome of DENV2 was replicated by ;4-fold at 25°and 37°C, which substantiates an earlier preliminary report. 34 Mock infected platelets had no detectable DENV RNA as a confirmation of qRT-PCR primer specificity (not shown). The effect of damaging the platelets by a prior freeze-thaw cycle was evaluated.…”

Section: Denv Genome Transcription By Plateletsmentioning

confidence: 86%

Dengue virus binding and replication by platelets

Simon

Sutherland

Pryzdial

2015

Blood

149

161

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Key Points• Platelets replicate and produce infectious DENV.• DENV binds directly to platelets using DC-SIGN and heparan sulfate proteoglycan as primary receptors.Dengue virus (DENV) infection causes ∼200 million cases of severe flulike illness annually, escalating to life-threatening hemorrhagic fever or shock syndrome in ∼500 000. Although thrombocytopenia is typical of both mild and severe diseases, the mechanism triggering platelet reduction is incompletely understood. As a probable initiating event, direct purified DENV-platelet binding was followed in the current study by quantitative reverse transcription-polymerase chain reaction and confirmed antigenically. Approximately 800 viruses specifically bound per platelet at 37°C. Fewer sites were observed at 25°C, the blood bank storage temperature (∼350 sites), or 4°C, known to attenuate virus cell entry (∼200 sites). Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) and heparan sulfate proteoglycan were implicated as coreceptors because only the combination of anti-DC-SIGN and lowmolecular-weight heparin prevented binding. Interestingly, at 37°C and 25°C, platelets replicated the positive sense single-stranded RNA genome of DENV by up to ∼4-fold over 7 days. Further time course experiments demonstrated production of viral NS1 protein, which is known to be highly antigenic in patient serum. The infectivity of DENV intrinsically decayed in vitro, which was moderated by plateletmediated generation of viable progeny. This was shown using a transcription inhibitor and confirmed by freeze-denatured platelets being incapable of replicating the DENV genome. For the first time, these data demonstrate that platelets directly bind DENV saturably and produce infectious virus. Thus, expression of antigen encoded by DENV is a novel consideration in the pathogen-induced thrombocytopenia mechanism. These results furthermore draw attention to the possibility that platelets may produce permissive RNA viruses in addition to DENV. (Blood. 2015;126(3):378-385)

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Section: Denv Genome Transcription By Plateletsmentioning

confidence: 86%

Dengue virus binding and replication by platelets

Simon

Sutherland

Pryzdial

2015

Blood

149

161

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“…Numerous primary cell lineages and established cell lines have been studied for their relative permissiveness for DENV and in vitro cellular responses have been used to elucidate virus-host interactions (Noisakran et al, 2010, Warke et al, 2003. The pathogenesis of dengue is also found to be complex, especially with the presence of four DENV serotypes which have been associated with disease severity and different virulence (Balmaseda et al, 2006;Nisalak et al, 2003;Vaughn et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Growth characteristics and cytokine/chemokine induction profiles of dengue viruses in various cell lines

Yohan¹,

Kendarsari²,

Mutia³

et al. 2014

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Summary. -The dengue disease varies clinically from mild fever to hemorrhagic fever up to potentially fatal shock syndrome. Such differences in manifestation of dengue virus (DENV) infection have been ascribed to intrinsic differences in DENVs. Four DENV serotypes or four dengue viruses (DENV-1 to DENV-4) have been clearly distinguished; however, only limited information is available on their biological characteristics in vitro. To shed more light on this subject, replication kinetics of all four DENVs in various cell lines and induction of 26 cytokines/chemokines were investigated. The results showed that, (i) all DENVs replicated relatively similarly in various cell lines, (ii) DENV-1 was most effective in this regard, (iii) A549 cells showed the highest virus replication rate compared to other cells, and (iv) all DENVs induced in A549 cells similar levels of several cytokines/chemokines, namely eotaxin, granulocyte colony stimulating factor (G-CSF), interferon alpha 2 (IFN-α2), interleukins 6, 8 15 (IL-6, IL-8, IL-15), and IP-10. In conclusion, this study revealed a similarity in growth characteristics and cytokine/chemokine induction profile for all four DENV serotypes in vitro.

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“…In general, immune cells with phagocytic capacity have been suggested to be infectable by DENV, especially cells with mannose-related receptors [15], DC-specific ICAM3-grabbing nonintegrin molecules [16], and CLEC5A [14] on the surface. However, recent evidence suggests that other immune cells, such as platelets and its precursor cells, megakaryocytes, are a favored target of DENV as well [17,18,19,20,21,22]. The latter may partially explain the dysfunction of platelets resulting in prolonged activated partial thromboplastin time (aPTT) during the early phase of dengue disease, and subsequent low platelet counts when the disease progresses to a critical stage [1].…”

Section: Introductionmentioning

confidence: 99%

Transient Monocytosis Subjugates Low Platelet Count in Adult Dengue Patients

Tsai

Chang

et al. 2017

Biomed Hub

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Background: Dengue is one of the most important vector-borne human viral diseases globally. The kinetic changes of hematological parameters of dengue in adult Taiwanese patients have seldomly been systematically investigated and characterized. Methodology/Principal Findings: Serial laboratory data of 1,015 adult patients who were diagnosed with dengue virus serotype 2 (DENV2) and 3 (DENV3) infections in southern Taiwan were retrospectively examined. Prominent parameters were verified with specimens from a 2015 dengue outbreak. Higher absolute monocyte counts on day 5 in severe patients than mild fever subjects after the onset of fever was seen. The absolute number of monocytes was significantly greater in those with DENV2 than DENV3 infections in spite of subtle differences in laboratory tests. Platelet counts were lowest and activated partial thromboplastin time was highest on day 5 in patients with severe conditions. In addition, sudden downward platelet counts corresponding to a transient surge of monocytes on day 4 onward was observed. Fluorescence-activated cell sorting analysis of peripheral blood mononuclear cells obtained from acute dengue patients and experimental investigations revealed that phagocytic effects of innate immune cells contribute to thrombocytopenia in dengue patients. Conclusion: Innate phagocytic cells play an essential role in low platelet counts in adult patients with dengue virus infections.

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Cells in Dengue Virus Infection In Vivo

Cited by 65 publications

References 136 publications

Dengue virus binding and replication by platelets

Dengue virus binding and replication by platelets

Growth characteristics and cytokine/chemokine induction profiles of dengue viruses in various cell lines

Transient Monocytosis Subjugates Low Platelet Count in Adult Dengue Patients

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