Finally, as it was recently shown that the privileged site of HIV replication during primary infection is the gastro-intestinal (GI) mucosa, and IgA could protect this mucosa, we verified whether the administration of CCL28 would result in a significant modulation of IgA in the GI tract using an animal model undergoing immunization with a VSV construct in the presence/absence of CCL28. This evidence concerns the gene CD79A and infection.