In conclusions, as for many epidemics, dealing with initial cases is often a key to successful subsequent management of further outbreaks. This case documents the experience of a public health physician as a patient in an infectious disease epidemic, with lessons for occupational and public health management. The lack of further transmission from this first case in the UAE may be a combination of good and effective public health intervention, or serendipity. Even though H1N1 has high infectivity with low case fatality rates, the number of cases globally declined, and WHO declared the end of the pandemic on 10 th August 2010. Human Anti-CCR4 Minibody Gene Transfer for the Treatment of Cutaneous T-Cell Lymphoma BACKGROUND: Although several therapeutic options have become available for patients with Cutaneous T-cell Lymphoma (CTCL), no therapy has been curative. Recent studies have demonstrated that CTCL cells overexpress the CC chemokine receptor 4 (CCR4). METHODOLOGY/PRINCIPAL FINDINGS: In this study, a xenograft model of CTCL was established and a recombinant adeno-associated viral serotype 8 (AAV8) vector expressing a humanized single-chain variable fragment (scFv)-Fc fusion (scFvFc or “minibody”) of anti-CCR4 monoclonal antibody (mAb) h1567 was evaluated for curative treatment. Human CCR4(+) tumor-bearing mice treated once with intravenous infusion of AAV8 virions encoding the h1567 (AAV8-h1567) minibody showed anti-tumor activity in vivo and increased survival. The AAV8-h1567 minibody notably increased the number of tumor-infiltrating Ly-6G(+) FcγRIIIa(CD16A)(+) murine neutrophils in the tumor xenografts over that of AAV8-control minibody treated mice. Furthermore, in CCR4(+) tumor-bearing mice co-treated with AAV8-h1567 minibody and infused with human peripheral blood mononuclear cells (PBMCs), marked tumor infiltration of human CD16A(+) CD56(+) NK cells was observed. The h1567 minibody also induced in vitro ADCC activity through both mouse neutrophils and human NK cells. CONCLUSIONS/SIGNIFICANCE: Overall, our data demonstrate that the in vivo anti-tumor activity of h1567 minibody is mediated, at least in part, through CD16A(+) immune effector cell ADCC mechanisms. These data further demonstrate the utility of the AAV-minibody gene transfer system in the rapid evaluation of candidate anti-tumor mAbs and the potency of h1567 as a potential novel therapy for CTCL. Cutaneous T cell lymphomas (CTCLs) are a clinically heterogeneous group of lymphoproliferative malignancies characterized by the clonal accumulation of mature and skin-homing memory T cells. Mycosis fungoides (MF), which is the most common and indolent form of CTCL, accounts for 50%-60% of CTCL cases [1] ; primary cutaneous CD30 + lymphoproliferative disorders, more specifically primary cutaneous anaplastic large cell lymphoma (PC-ALCL) -the second most common CTCL, accounts for circa 30%; and Sézary syndrome, which is an aggressive leukemic variant of CTCL, affects approximately 5% of patients. These patients exhibit significant immune dysfunction [2, 3] because of the global dysregulation of T cells, which is due to an unknown etiology [4, 5] . Bacterial sepsis is the terminal event in most patients with advanced cancer. Current therapies for patients with advanced CTCL, including its leukemic variant, are only palliative, and extensive long-term remissions are rare. The poor 5-year survival rate of these patients receiving existing therapies clearly emphasizes the need for the development of new targeted therapies in this fatal disease [6] .