Rôle du placenta dans la transmission mère-enfant du VIH

La transmission mère-enfant est la première cause d’infection par le virus de l’immunodéficience humaine (VIH) chez l’enfant. Chez les nourrissons et les enfants, on considère que plus de 90 % des nouvelles infections surviennent suite à une transmission mère-enfant du VIH. En l’absence de toute intervention, entre 20 % et 45 % des nourrissons peuvent se trouver infectés, le risque étant estimé à 5 à 10 % pendant la grossesse, 10 à 20 % pendant le travail et l’accouchement, et 5 à 20 % au cours de l’allaitement maternel. Grâce aux cultures de cellules trophoblastiques et aux techniques de mesure des cytokines, les mécanismes de protection mis en jeu lors du passage transplacentaire du VIH durant la grossesse sont mieux connus.

 

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Données épidémiologiques sur la transmission mère-enfant

Selon les chiffres de l’Organisation mondiale de la santé (OMS), 17,7 millions de femmes et 2,3 millions d’enfants de moins de 15 ans étaient infectés par le VIH en 2006. Dans les pays les plus touchés d’Afrique subsaharienne, les femmes, les nourrissons et les jeunes enfants représentent plus de 60 % de toutes les nouvelles infections à VIH. Les femmes enceintes vivant avec le VIH ont un risque élevé de transmission du VIH à leurs enfants, au cours de la grossesse, de l’accouchement ou pendant l’allaitement au sein.

Structure du placenta

Le placenta est un organe qui représente une surface de contact et d’échanges de 10m2 entre la mère et l’enfant. Il sépare les deux systèmes sanguins maternel et foetal, est responsable des échanges nutritionnels et gazeux et constitue pour le foetus une barrière contre les agents infectieux, notamment le virus de la rubéole, le cytomégalovirus, le VIH et le virus de l’hépatite B.
En ce qui concerne la transmission du VIH, une étude [1] publiée dans The Lancet montre que seuls 15 à 30% des nouveau-nés de femmes séropositives seront contaminés (hors transmission ultérieure par l’allaitement), sous-entendant ainsi l’existence de facteurs de protection.
Il est maintenant clairement établi que le placenta joue le rôle d’une véritable barrière contre les agents infectieux. En effet, grâce aux techniques d’immunohistochimie, d’hybridation in situ [2] et de PCR [3] , on peut facilement détecter l’ADN viral dans le placenta. Les différentes observations montrent que l’on détecte la présence d’ADN viral dans 100% des placentas à terme de femmes séropositives, suggérant bien que le placenta joue le rôle de filtre vis à vis du VIH.

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Placenta

Les tissus maternels et foetaux s’organisent en deux entités étroitement intriquées au niveau du placenta :
La partie foetale du placenta est constituée par la plaque choriale avec les villosités placentaires, la coque cytotrophoblaste et les espaces intervilleux. La plaque choriale, partie profonde du placenta du côté foetal est formée de l’amnios, du mésenchyme extra-embryonnaire, du cytotrophoblaste et du syncytiotrophoblaste.

La plaque basale, partie externe du placenta au contact de la paroi utérine, d’origine composite, formée par des tissus embryonnaires (cytotrophoblaste, syncytiotrophoblaste) et des tissus maternels (caduque basilaire).

La partie maternelle du placenta est elle constituée par la caduque basilaire, les vaisseaux et les glandes utérines.

Sélection des variants viraux

La transmission verticale du VIH 1 est caractérisée par la sélection de variants génotypiques qui échappent au système immunitaire maternel.

Selon les études publiées, il semble que seuls quelques variants viraux passent la barrière transplacentaire. Si l’on compare les variants viraux présents dans le placenta avec ceux des cellules mononuclées du sang périphérique de la mère, on s’aperçoit que déjà au niveau placentaire, la variabilité virale est réduite, avec prédominance de virus à tropisme macrophagique.

Mécanismes de la transmission du VIH

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Placenta Anatomy Atlases

- Modulation du transport et de la transcytose
Les cellules trophoblastiques du placenta sont considérées comme une cible potentielle du rétrovirus ou serviraient éventuellement au passage du VIH vers le fœtus (transcytose). Ces cellules permettraient ainsi le passage du VIH, non pas via des microlésions ou brèches (mécanisme mineur de transmission) apparaissant dans la couche trophoblastique placentaire surtout en fin de grossesse, mais directement par le biais de son internalisation par les trophoblastes.

Le processus de transmission du VIH par infection ou transcytose serait favorisé, ou encore inhibé, par des facteurs liés à la fois au phénotype viral mais également à l’environnement cellulaire.

- Modulation de l’expression des co-récepteurs
La transmission verticale du VIH peut être médiée par les CD4+ maternels dans la mesure où le trophoblaste et les villosités choriales possèdent des récepteurs aux CD4+. Il semble toutefois qu’il existe une modulation de l’expression des récepteurs CD4, des co-récepteurs majeurs (CCR5 et CXCR4) du VIH-1 sur les cellules trophoblastiques en fonction de leur stade de différenciation ; cette expression étant plus importante en début de grossesse qu’à l’approche du terme.

- Modulation de la réplication dans le trophoblaste

Cytokines et chémokines
Des cytokines et des chémokines placentaires semblent par ailleurs influencer la réplication du VIH dans le trophoblaste. Pendant la période de gestation, le placenta et le foetus expriment une quantité d’hormones, de facteurs de croissance et de cytokines qui agissent sur les fonctions placentaires et la croissance des cellules du placenta en les modulant.

Les cytokines
En ce qui concerne les cytokines exprimées en cours de grossesse, les concentrations de TNF-α (tumor necrosis factor) d’IL-1β et d’IL-6 (interleukines-1β et 6) sont plus élevées dans le placenta des femmes infectées par le VIH. De plus, il existe une corrélation positive entre le taux d’expression de TNF-α par les cellules trophoblastiques et le taux de transcription du VIH.

Il apparaît donc au vu de ces résultats que les cytokines ou les facteurs de croissance, présents dans l’environnement placentaire et dont l’expression est modulée dans le temps, pourraient jouer un rôle important dans la régulation du cycle de réplication du VIH et la susceptibilité des trophoblastes au VIH.

En d’autres termes, selon leur nature, les cytokines pourraient favoriser une infection productive par le VIH ou, au contraire, conférer une certaine protection contre l’infection. Dans cette optique, il est intéressant de noter que les cytokines IL-1 et TNF-α, activatrices de l’expression virale, sont exprimées par le placenta en début de grossesse puis au moment de l’accouchement, deux stades correspondant précisément aux périodes où les risques de transmission mère-enfant sont les plus élevés.

Les chimiokines
Certaines chimiokines se conduisent comme des facteurs suppresseurs de la réplication du VIH :
- MIP-1 (Macrophage inflammatory protein) alpha, bêta ;
- Rantes (regulated upon activation, normal T cell expressed and secreted) [4] ;
- SDF-1 (Stromal-Derived Factor-1).

Autres facteurs "anti-réplicateurs" du VIH
- LIF (leukemia inhibitory factor)
Les femmes qui, infectées par le VIH, n’ont pas transmis le virus à leur nouveau-né, ont une concentration placentaire plus élevée d’ARNm de LIF [5] que les femmes VIH+ qui transmettent l’infection.

- La β1-défensine
Un article récent a établi un lien entre le polymorphisme génétique de la β1-défensine [6]. et la transmission verticale du VIH. Chez l’enfant le génotype -52GG et l’haplotype -44G/652G auraient un rôle protecteur vis à vis de l’infection à VIH. Chez la mère, ce variant génétique serait associé à une charge virale inférieure à 1000 copies par mL et à un risque plus faible de transmission materno-foetal.

- L’HcG (Human Chorionic Gonadotropin)
L’HcG [7], hormone secrétée par le placenta a été identifiée conmme étant un facteur suppresseur de la transmission du VIH.

Conclusion
Il apparaît que la transmission transplacentaire du VIH dépend de mécanismes de régulation liés à la fois aux cellules trophoblastiques placentaires et aux caractéristiques fonctionnelles et structurales propres aux variants viraux. La transmission mère-enfant du VIH ne peut avoir lieu que si un ensemble d’éléments associés aux facteurs d’origine virale et de l’hôte sont réunis. La compréhension de l’ensemble des mécanismes intervenant dans ce processus est en progrès depuis quelques années et devrait permettre d’établir de nouvelles stratégies pour contrer la transmission verticale du VIH.

Source :
- Role of placenta in the vertical transmission of human immunodeficiency virus
Al-Husaini AM.
J Perinatol. 2009 May ;29(5):331-6.

- Maternal neutralizing antibodies against a CRF01_AE primary isolate are associated with a low rate of intrapartum HIV-1 transmission.
Samleerat T, Thenin S, Jourdain G, Ngo-Giang-Huong N, Moreau A, Leechanachai P, Ithisuknanth J, Pagdi K, Wannarit P, Sangsawang S, Lallemant M, Barin F, Braibant M.
Virology. 2009 May 10 ;387(2):388-94

-  Role of beta-defensin-1 polymorphisms in mother-to-child transmission of HIV-1.
Ricci E, Malacrida S, Zanchetta M, Montagna M, Giaquinto C, De Rossi A.
J Acquir Immune Defic Syndr. 2009 May 1 ;51(1):13-9

- Vers une compréhensiondu mécanisme de transmission du VIH in utero
Vidricaire, Michel J. Tremblay
MEDECINE/SCIENCES 2004 ; 20 : 784-7

- La barrière placentaire
Gérard Chaouat, Marlène Moussa, Juan Maldonado, Elisabeth Menu
Revue Française des Laboratoires Volume 2003, Issue 353, May 2003, Pages 21-28

- Detection of human defensins in the placenta
SVINARICH D. M. ; GOMEZ R. ; ROMERO R.
Annual Meeting of the Society for Gynecological Investigation No44, San Diego, California , ETATS-UNIS (19/03/1997) 1997, vol. 38, no 4, pp. 237-312 (10 ref.), pp. 252-255

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