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ReplyLetter

Dr. Roimicher, et al, reply

LUIS ROIMICHER, ORLANDO C. FERREIRA JR., MONICA B. ARRUDA and AMILCAR TANURI
The Journal of Rheumatology March 2018, 45 (3) 444; DOI: https://doi.org/10.3899/jrheum.171089
LUIS ROIMICHER
Department of Rheumatology, Hospital Universitário Clementino Fraga Filho (CFF), Universidade Federal do Rio de Janeiro;
MD, PhD
Roles: Professor of Rheumatology
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  • For correspondence: mail-luizroimicher{at}gmail.com
ORLANDO C. FERREIRA JR.
Laboratory of Molecular Virology, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
MD, PhD
Roles: Professor
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MONICA B. ARRUDA
Laboratory of Molecular Virology, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
PhD
Roles: Professor
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AMILCAR TANURI
Laboratory of Molecular Virology, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
MD, PhD
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To the Editor:

We read the letter from Colavita, et al1, where the authors show by in vitro experiments that human osteoblast-like SV-40 T antigen immortalized (HOBIT) cells are productively infected by Zika virus (ZIKV). Their experiments with HOBIT cells infected with both Asian and African Zika strains show that both viruses are indeed able to produce a fair amount of virus 96 h postinfection. It is interesting that ZIKV could replicate in a HOBIT cell line and that we can find this kind of cell in normal articular tissue. A direct translation of their results to the case reported by us2 has to be put into perspective, however.

For instance, in the case presented by our group, a woman with rheumatoid arthritis (RA) had been in therapy-induced clinical remission for 4 months before being infected with ZIKV. The patient then presented with arthralgia and a clinical picture suggestive of ZIKV infection, which was confirmed by the presence of ZIKV genetic material in her knee synovial fluid by reverse transcriptase–PCR, even after the virus disappeared from her blood. Although the patient was in clinical remission for RA, her articular space could have been infiltrated by inflammatory cells such as macrophages, as well as activated lymphocytes that could be the major target cells for ZIKV replication. In ZIKV vertical transmission, human macrophages can be implicated because the virus has been detected in placental tissues of infected expectant mothers, specifically within the placental macrophages, known as Hofbauer cells, and intervillous histiocytes found on the maternal side3,4. Additionally, the neurotropism of ZIKV for glial cells and endothelial cells of fetal brains has also been identified4.

Nevertheless, the finding of direct infection of osteoblast cells by ZIKV reported by Colavita, et al1 offers an interesting alternative hypothesis for the arthritis caused by ZIKV infection. However, more work is needed to show what kind of cell cooperates with viral replication in the joint during the arthritis episodes induced by ZIKV infection. Immunohistochemistry analysis performed with specific monoclonal antibodies against ZIKV in cells found in a joint cavity of patients affected with clinical arthritis after ZIKV infection could help us to find the nature of cells infected by ZIKV.

REFERENCES

  1. 1.↵
    1. Colavita F,
    2. Musumeci G,
    3. Caglioti C
    . Human osteoblast-like cells are permissive for Zika virus replication. J Rheumatol 2018;45:443–4.
    OpenUrlFREE Full Text
  2. 2.↵
    1. Roimicher L,
    2. Ferreira OC Jr,
    3. Arruda MB,
    4. Tanuri A
    . Zika virus in the joint of a patient with rheumatoid arthritis. J Rheumatol 2017;44:535–6.
    OpenUrlFREE Full Text
  3. 3.↵
    1. Jurado KA,
    2. Simoni MK,
    3. Tang Z,
    4. Uraki R,
    5. Hwang J,
    6. Householder S,
    7. et al.
    Zika virus productively infects primary human placenta-specific macrophages. JCI Insight 2016;1(13)e88461.
    OpenUrl
  4. 4.↵
    1. Noronha Ld,
    2. Zanluca C,
    3. Azevedo ML,
    4. Luz KG,
    5. Santos CN
    . Zika virus damages the human placental barrier and presents marked fetal neurotropism. Mem Inst Oswaldo Cruz 2016;111:287–93.
    OpenUrlCrossRef
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The Journal of Rheumatology
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1 Mar 2018
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Dr. Roimicher, et al, reply
LUIS ROIMICHER, ORLANDO C. FERREIRA, MONICA B. ARRUDA, AMILCAR TANURI
The Journal of Rheumatology Mar 2018, 45 (3) 444; DOI: 10.3899/jrheum.171089

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Dr. Roimicher, et al, reply
LUIS ROIMICHER, ORLANDO C. FERREIRA, MONICA B. ARRUDA, AMILCAR TANURI
The Journal of Rheumatology Mar 2018, 45 (3) 444; DOI: 10.3899/jrheum.171089
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