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Since the emergence of Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012 (1), more than 2,250 laboratory-confirmed cases have been reported to the World Health Organization (WHO); approximately one third [...]

Middle East respiratory syndrome coronavirus (MERS-CoV) was identified in 2012 in a cell culture taken from a patient who died of pneumonia in Saudi Arabia (1). Since 2012, at least [...]

The Middle East respiratory syndrome coronavirus (MERS-CoV) is a zoonotic pathogen that causes severe respiratory disease in humans. Dromedary camels (Camelus dromedarius), which have 1 hump on their backs, have [...]

To the Editor: In 2012, a novel coronavirus termed Middle East respiratory syndrome coronavirus (MERS-CoV) emerged on the Arabian Peninsula; the virus has been responsible for >800 human cases. Recently, [...]

Background. The Middle East respiratory syndrome (MERS) coronavirus causes isolated cases and outbreaks of severe respiratory disease. Essential features of the natural history of disease are poorly understood. Methods. We studied 37 adult patients infected with MERS coronavirus for viral load in the lower and upper respiratory tracts (LRT and URT, respectively), blood, stool, and urine. Antibodies and serum neutralizing activities were determined over the course of disease. Results. One hundred ninety-nine LRT samples collected during the 3 weeks following diagnosis yielded virus RNA in 93% of tests. Average (maximum) viral loads were 5 × 106 (6 × 1010) copies/mL. Viral loads ( positive detection frequencies) in 84 URT samples were 1.9 × 104 copies/mL (47.6%). Thirty-three percent of all 108 serum samples tested yielded viral RNA. Only 14.6% of stool and 2.4% of urine samples yielded viral RNA. All seroconversions occurred during the first 2 weeks after diagnosis, which corresponds to the second and third week after symptom onset. Immunoglobulin M detection provided no advantage in sensitivity over immunoglobulin G (IgG) detection. All surviving patients, but only slightly more than half of all fatal cases, produced IgG and neutralizing antibodies. The levels of IgG and neutralizing antibodies were weakly and inversely correlated with LRT viral loads. Presence of antibodies did not lead to the elimination of virus from LRT. Conclusions. The timing and intensity of respiratory viral shedding in patients with MERS closely matches that of those with severe acute respiratory syndrome. Blood viral RNA does not seem to be infectious. Extrapulmonary loci of virus replication seem possible. Neutralizing antibodies do not suffice to clear the infection. [ABSTRACT FROM AUTHOR]