The American Plague - Molly Caldwell Crosby [4]
Yellow fever is what is known as a flavivirus, a group of viruses spread by mosquitoes that includes West Nile, dengue and Japanese encephalitis. As a virus, yellow fever is not one of the stronger ones. It cannot live outside of the body for more than a few hours. It does not spread through the air or by touch. It does not mutate as easily as some viruses. In fact, its most telling symptom—fever—is really just the body’s own attempt to kill the virus. What makes yellow fever unique is its choice of vector. What the virus lacks in evolutionary prowess, the mosquito makes up for.
In the African rain forest, mosquitoes carry the virus, this finely evolved life-form looking to conquer. The mosquito feeds off of the monkeys in the tree canopy, and a small epidemic erupts, foreshadowing the larger one to follow.
Of course, none of this would be known until well into the twentieth century. For the Africans and Europeans, and later for the Americans, a virus would remain an invisible, unknown entity. No one would even know how yellow fever spread from one person to the next until 1900.
As the men made their way back to the Niger Delta and the coast of West Africa where the timber would be sold for ships carrying palm oil, ivory, salt, gold and slaves, they might run a mild fever or feel lethargic, but it was nothing compared to what the white Europeans would feel in the coming weeks. Through this cycle of men entering the forests, mosquitoes biting men and the virus spreading among small tribal villages, most native Africans had encountered the yellow fever virus at one time or another. They acquired immunity to it, and the virus began to run out of the kindling that kept the flames of fever alive. When white Europeans landed on the coast of West Africa, it was like a fresh burst of oxygen in a waning fire.
The Nigerian coast had been booming with the slave trade since the fifteenth century, providing the Middle Passage across the Atlantic with 30 percent of its human exports. As the ships of the Portuguese, Spanish, Dutch and English pitched in the ocean swells along the coast, they waited for the cargo making its way from the interior down the river delta to the coast.
The port towns were filled with the smells of Africa: sweet oil from the palms, spices, yams and dates sold at local markets. There was fire smoke and the poignant scent of rainwater mixed with human sweat where the next shipment of slaves sat chained to one another in thatched sheds, waiting to board the ship. Fearful of tropical diseases, the Europeans might even taste the sweat of slaves to try to determine if he or she carried disease. The smells would worsen in the next few months at sea when hot air, sweat and human excrement would be trapped beneath deck with the slaves. When the ships encountered squalls, and the sea and sky would join, the tumbling ship would induce vomit to add to the amalgam of human smells.
As the ship traversed the waters of the Atlantic, the virus made its way through the bloodstream of the passengers as succinctly as it had made its way through the rivers of West Africa to the coast. In the blood, yellow fever looks something like a fuzzy snowflake, but it is actually round with twenty smooth sides that protect the virus’s single strand of RNA at the center. The coating of the virus is made up of proteins, and human cells are attracted to those proteins—the virus doesn’t need to look for healthy cells; they look for it. Once the two make contact in the bloodstream, a process with a technical name known as receptor-mediated endocytosis begins—sort of a molecular Trojan horse. The healthy cell eventually enfolds the virus, taking it in and closing the door behind it. Once inside, the virus hijacks the cell and its basic machinery, using the cell’s internal makeup to replicate the viral proteins and RNA, until the new particles burst through the cell. A body that was once filled with healthy cells is now