Prostaglandin A<sub>1</sub> inhibits the replication of bovine viral diarrhea virus

Bovine viral diarrhea virus can cause acute disease in livestock, leading to economic losses. We show that Prostaglandin A₁ inhibits bovine viral diarrhea virus replication in Madin-Darby bovine kidney cells (94% inhibition using 5 µg/mL). Light and electron microscopy of infected cells shows that Prostaglandin A₁ also prevents virus-induced vacuolization, but at higher concentrations (10 µg/mL).

Keywords:
Bovine viral diarrhea virus; BVDV; Prostaglandins; Prostaglandin A1; Virus-induced vacuolization

Authorship

Lúcio Ayres Caldas ^**Corresponding author at: Universidade Federal do Rio de Janeiro, Instituto de Biofísica Carlos Chagas Filho, Laboratório de Ultraestrutura Celular Hertha Meyer, Rio de Janeiro, RJ, Brazil. E-mail: lucio@biof.ufrj.br (L.A. Caldas).

Instituto Nacional de Metrologia, Qualidade e Tecnologia (INMETRO), Rio de Janeiro, RJ, BrazilInstituto Nacional de Metrologia, Qualidade e TecnologiaBrazilRio de Janeiro, RJ, BrazilInstituto Nacional de Metrologia, Qualidade e Tecnologia (INMETRO), Rio de Janeiro, RJ, Brazil

Tânia Rosária Pereira Freitas

Ministério da Agricultura, Pecuária e Abastecimento, Laboratório Nacional Agropecuário – LANAGRO – MG, Pedro Leopoldo, MG, BrazilMinistério da Agricultura, Pecuária e AbastecimentoBrazilPedro Leopoldo, MG, BrazilMinistério da Agricultura, Pecuária e Abastecimento, Laboratório Nacional Agropecuário – LANAGRO – MG, Pedro Leopoldo, MG, Brazil

Renata Campos Azevedo

Universidade Federal do Rio de Janeiro, Instituto de Microbiologia Professor Paulo de Góes, Rio de Janeiro, RJ, BrazilUniversidade Federal do Rio de JaneiroBrazilRio de Janeiro, RJ, BrazilUniversidade Federal do Rio de Janeiro, Instituto de Microbiologia Professor Paulo de Góes, Rio de Janeiro, RJ, Brazil

Wanderley de Souza

Universidade Federal do Rio de Janeiro, Instituto de Biofísica Carlos Chagas Filho, Rio de Janeiro, RJ, BrazilUniversidade Federal do Rio de JaneiroBrazilRio de Janeiro, RJ, BrazilUniversidade Federal do Rio de Janeiro, Instituto de Biofísica Carlos Chagas Filho, Rio de Janeiro, RJ, Brazil

*Corresponding author at: Universidade Federal do Rio de Janeiro, Instituto de Biofísica Carlos Chagas Filho, Laboratório de Ultraestrutura Celular Hertha Meyer, Rio de Janeiro, RJ, Brazil. E-mail: lucio@biof.ufrj.br (L.A. Caldas).

Associate Editor: Fernando Spilki

SCIMAGO INSTITUTIONS RANKINGS

Figures | Tables

Figures (2)
Tables (1)

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Fig. 1
Light microscopy analysis of bovine viral diarrhea virus (BVDV) infected cells treated with prostaglandin A₁ (PGA₁). MDBK cells were treated with PGA₁ for 36 h, and then subjected to panoptic staining. Low and high magnification images of untreated mock-infected cells (A, B), and of infected cells kept untreated (C, D) or treated with 5 (E) and 10 (F) µg/mL PGA₁. Although 5 µg/mL PGA₁ strongly blocked BVDV replication (E), it did not inhibit the vacuolization process (arrows). Vacuolization inhibition was only achieved after treatment with 10 µg/mL PGA₁ (F). Scale bars: 8 µm.

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Fig. 2
Transmission electron microscopy (TEM) analysis of bovine viral diarrhea virus (BVDV)-infected cells treated with prostaglandin A₁ (PGA₁). Infected and non-infected MDBK cells were treated with PGA₁ for 36 h, and then processed for routine TEM. Vacuoles (v) were rare or absent in the majority of sections from non-infected cells (A), but were abundant in BVDV-infected cells not treated with PGA₁ (B). Many of these structures exhibited extracellular content, as shown by ruthenium red labeling (arrows) in traditional (C) and en face (D) sections. Treatment with 1 µg/mL (E) or 2.5 µg/mL (F) PGA₁ could not prevent BVDV-induced vacuolization in infected cells, which had large vacuoles (arrows) with multilamellar structures (arrowheads), and often surrounded by smaller vesicles-containing vacuoles (thin arrows). (G) Treatment with 10 g/mL PGA₁, however, dramatically reduced virus-induced vacuolization. n, nucleus. Scale bars: (A) 5 µm; (B, G) 2 µm; (C, E) 500 nm; (D, F) 1 µm.

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Table 1
Effect of prostaglandin A₁ (PGA₁) on bovine viral diarrhea virus (BVDV) replication in MDBK cells, expressed as the TCID₅₀ and the percentage of replication inhibition.

Fig. 1 Light microscopy analysis of bovine viral diarrhea virus (BVDV) infected cells treated with prostaglandin A₁ (PGA₁). MDBK cells were treated with PGA₁ for 36 h, and then subjected to panoptic staining. Low and high magnification images of untreated mock-infected cells (A, B), and of infected cells kept untreated (C, D) or treated with 5 (E) and 10 (F) µg/mL PGA₁. Although 5 µg/mL PGA₁ strongly blocked BVDV replication (E), it did not inhibit the vacuolization process (arrows). Vacuolization inhibition was only achieved after treatment with 10 µg/mL PGA₁ (F). Scale bars: 8 µm.

Fig. 2 Transmission electron microscopy (TEM) analysis of bovine viral diarrhea virus (BVDV)-infected cells treated with prostaglandin A₁ (PGA₁). Infected and non-infected MDBK cells were treated with PGA₁ for 36 h, and then processed for routine TEM. Vacuoles (v) were rare or absent in the majority of sections from non-infected cells (A), but were abundant in BVDV-infected cells not treated with PGA₁ (B). Many of these structures exhibited extracellular content, as shown by ruthenium red labeling (arrows) in traditional (C) and en face (D) sections. Treatment with 1 µg/mL (E) or 2.5 µg/mL (F) PGA₁ could not prevent BVDV-induced vacuolization in infected cells, which had large vacuoles (arrows) with multilamellar structures (arrowheads), and often surrounded by smaller vesicles-containing vacuoles (thin arrows). (G) Treatment with 10 g/mL PGA₁, however, dramatically reduced virus-induced vacuolization. n, nucleus. Scale bars: (A) 5 µm; (B, G) 2 µm; (C, E) 500 nm; (D, F) 1 µm.

Table 1 Effect of prostaglandin A₁ (PGA₁) on bovine viral diarrhea virus (BVDV) replication in MDBK cells, expressed as the TCID₅₀ and the percentage of replication inhibition.

PGA₁ concentration (µg/mL)	TCID₅₀/mL	% Inhibition
0	1 × 10⁵	0
0.5	5.6 × 10⁴	44
1.0	5.0 × 10⁴	50
2.5	1.9 × 10⁴	81
5	6.3 × 10³	94

MDBK cells were infected with BVDV and treated with different concentrations of PGA₁. The percentage of BVDV replication inhibition was calculated by measuring the virus yield in the supernatant of infected cells 36 h after PGA₁ treatment. While 1.0 µg/mL PGA₁ inhibited 50% of BDVD production, the highest concentration tested in this assay (5 µg/mL PGA₁) blocked replication by >90%.

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Sociedade Brasileira de Microbiologia USP - ICB III - Dep. de Microbiologia, Sociedade Brasileira de Microbiologia, Av. Prof. Lineu Prestes, 2415, Cidade Universitária, 05508-900 São Paulo, SP - Brasil, Ramal USP 7979, Tel. / Fax: (55 11) 3813-9647 ou 3037-7095 - São Paulo - SP - Brazil
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